Exam 2 Flashcards

1
Q

What coordinates reflex control of BP and blood distribution

A

CNS

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2
Q

Medulla oblongata (brain stem)

A

Major integrating center
Monitors flow NOT pressure via stretch receptors

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3
Q

Cardiovascular Control Center (CVCC)

A

Receives input from central and peripheral receptors
Hypothalamus, baroreceptors (stretch) in aorta and carotid and intestinal tract
Constant monitoring and adjusting

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4
Q

If BP decreases what happens to symp output

A

Increases
Because causes vasoconstriction which will increase BP

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5
Q

Baroreceptor reflex regulating MAP

A

Stretch receptors in aorta and carotid
Send action potentials to CVCC
Change in BP = change in AP frequency
(ex: Increase BP = increased stretch = frequency of AP)
CVCC response to barorecep. alters CO and Resistance in arterioles
See diagram 15.5 slide 47

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6
Q

How do baroreceptors operate when we exercise?

A

Baroreceptors reset during exercise to regulate BP around a higher set point.

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7
Q

Orthostatic hypotension

A

AKA stand up too fast and see spots
Standing up causes blood to pool in lower body due to gravity
Decreased blood in ventricles due to decreased venous return
CO falls
BP falls
MAP increases (Baroreceptors) within 2 heartbeats

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8
Q

Factors that influence CV function

A

Peripheral chemoreceptors, respiratory control centers
Higher brain centers
Fluid balance

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9
Q

Peripheral chemoreceptors

A

Aterial O2 receptors

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10
Q

Respiratory control centers

A

Sends info to CVCC

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11
Q

Higher brain centers

A

Hypothalamus- body temp, symp activation
Cerebral cortex- learned or emotional factors (choose to hold breath, fear, surprise)

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12
Q

Vasovagal syncope

A

Fainting from strong parasymp release (drops HR and BP)
Body overreact to seeing blood or extreme distress

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13
Q

Fluid balance

A

Renal and CV systems highly integrated to regulate fluids

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14
Q

Capillary network

A

50,000 miles
Metabolic activity of tissue influences density of capillary network

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15
Q

Capillary structure

A

Single layer of flat endothelial cells (EC)
Diameter slightly larger than RBC
Cell junctions determine leakiness

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16
Q

Continuous capillaries

A

Most common
Leaky junctions (least leaky capillary tho)
Found in muscle, connective, and neural tissue except brain (blood brain barrier needs thicker capillaries to keep out bad from brain)

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17
Q

Fenestrated capillaries

A

Larger pores between ECs
Promote high volume fluid exchange
Kidney and intestine

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18
Q

Sinusoids

A

Modified capillaries
Bone marrow, liver, spleen
five times wider than normal capillaries
Allow RBC and plasma proteins to cross into blood

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19
Q

Why is velocity of blood lowest in arterioles, caps, and venules even tho they are skinniest?

A

These vessels have the largest cross sectional area so blood is spread out and therefore slower through network

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20
Q

Why do you want capillaries to have a slower blood velocity

A

Promotes exchange

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21
Q

Diffusion

A

Gradient driven exchange

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22
Q

Transcytosis

A

Larger molecules transported through EC

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23
Q

Paracellular

A

larger molecules move between EC pores

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24
Q

Typical endothelial cell junctions of continuous caps allow for

A

allow water and small dissolved solutes to pass

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25
Absorption
Fluid moves into capillary; determined by bulk flow
26
Filtration
Fluid leaves capillary; determined by bulk flow
27
Hydrostatic pressure (BP)
lateral pressure of fluid through pores
28
Osmotic pressure
Determined by solute concentration of fluid; protein concentration in blood --> Colloid osmotic pressure
29
Fluid movement in capillary
Arteriole end: Hydrostatic pressure greater than colloid osmotic, so fluid is pushed out of cap = filtration Venule end: colloid osmotic greater than hydrostatic, so fluid enters cap (water attracted to proteins) = absorption Net flow out of cap (3L/day)
30
Why is colloid osmotic pressure constant from arteriole to venule
Because proteins aren't moving in and out of blood
31
Lymphatic system
Returns the lost fluid back to the blood via emptying into venous system (Vena cava); not a closed loop
32
Thymus
Adaptive immune system, T-cells mature, detect if self or not Atrophies with age because u are exposed to less new stuff
33
Spleen
Activation site of immune system Recycle dead RBCs Reservoir for RBCS Can live without -> weak immune system
34
Lymphatic system interaction with other systems
CV system- returns fluid lost in capillaries Digestive- transport of lipids to CV Immune- recognition and destruction of foreign pathogens
35
Lymph Vessels
Blind ended vessels, lie close to capillaries Thin flat endothelium Very porous- protein, cell, bacteria can enter
36
Larger lymphatic vessels
Semilunar valves to prevent backflow, empty into venous subclavian and internal jugular
37
Lymph nodes
Activation of immune system Fibrous bean nodes Macrophages and lymphocytes Antigen recognition
38
Other structures of lymph system
Spleen, thymus, gut-associated lymph tissue
39
Edema
Accumulation of fluid in interstitial space Inadequate drainage of lymph- protein accumulation in interstitial place Excessive capillary filtration- increased permeability of caps
40
Three factors that disrupt capillary filtration
1. Increase capillary BP (more fluid exits and less can come back in) 2. Decrease plasma protein concentration (increased fluid loss due to less absorption, cause by malnutrition and liver failure) 3. Increased interstitial proteins (Increased capillary permeability, cause by infection/damage)
41
Components of blood
Plasma (Fluid)- water, ions, organic molecules, elements, vitamins, gases Cellular elements (White & red blood cells, platelets)
42
Plasma
ECM Majority water (92%) 7% protein, 1% dissolved organic substances Similar to Interstitial fluid but with proteins Proteins increase osmotic pressure
43
Plasma proteins
Albumin (largest component) Globulins (antibodies) Fibrinogen Transferrin
44
RBCs
Erythrocytes Lack mitochon, ER, and nucleus so there is more room for gasses to transport only energy source is glucose via glycolysis Can't replicate --> short life
45
White blood cells
Leukocytes Only fully functional blood cell Critical for immune function/defense
46
5 types of WBCs
Lymphocytes, monocytes, neutrophils, eosinophils, basophils
47
Platelets
Thrombocytes Critical for hemostasis Lack nucleus Fragments of megakaryocytes so not a living cell NSAIDs knock out platelets
48
Hematopoietic Stem Cell
Found in bone marrow (primarily long bones) Pluripotent- can develop into RBC, WBC, or platelets
49
Hematopoiesis
Synthesis of blood cells Occurs in embryonic and postnatal environments
50
Complete Blood count (CBC)
Analysis of blood components Compare blood cell numbers to normal ranges Indicator of health conditions
51
Hematocrit
Percentage of RBCs in total blood volume 40-54% Males 37-47% Females Lower in females because of weight/BV
52
Hemoglobin
Oxygen carrying capacity of RBCs Units: g Hb/dL 14-17 Males 12-16 Females
53
Red cell count
Count of erythrocytes as they stream through beam of light Units: cells/uL 4.5-6.5E6 Males 3.9-5.6E6 Females
54
Total white cell count
Shoes overall immune response, don't need to know #s
55
Shape of RBCs
Biconcave disc Increase SA which increases gas exchange
56
Erythrocytes (RBCs)
Most abundant cell in blood 5 mil RBCs/uL blood Primary role to carry O2 and CO2 Lack nucleus, ER, mitochondria Biconcave More flexible (to bounce around vessels Packed with Hb
57
Hemoglobin (Hb)
4 heme groups bind together to create 1 Hb Major component of RBC
58
Heme group
Binds O2 and CO2 Has 1 iron Contains 70% of body's iron Subunit of Hb
59
Transferrin
Protein that transports iron in the plasma
60
Ferritin
cells' storage of excess iron, mostly in liver Extra can be toxic
61
Iron Transport
1. iron ingested 2. Fe absorbed by active transport 3. Transferrin transports Fe in plasma 4. Bone marrow uses Fe to make Hb as RBC synth 5. RBCs live for 90-120 days 6. Spleen destroys RBC and converts Hb to bilirubin 6. Bilirubin and metabolites excreted in urine and feces OR after step 3 4b. Liver stores excess Fe as ferritin 5b. Liver metabolizes bilirubin and excretes it in bile
62
Hyperbilirubinemia
Elevated bilirubin Jaundice Infants- fetal Hb accumulation (liver not fully developed) Adults- liver disease/dysfunc.
63
Anemia
Hb count too low Causes: Blood loss, Hemolysis (RBCs explode), Acquired (infection, drugs, disease), Radiation, low Fe folic acid or B12 intake, Low erythropoietin levels
64
Thrombocytes (Platelets)
Cell fragments of megakaryocytes Critical for reducing blood loss, lack a nucleus, contain granules that contain cytokines and growth factors (many proteins and chemicals), live ~10 days
65
Challenges to the repair process
Can't occlude the entire vessel because nutrients and gasses need to get downstream Blood is under pressure so the repair must be strong to withstand the shear stress Repair can't be permanent cuz clots affect MAP
66
3 stages of Hemostasis
Vasoconstriction Formation of platelet plug Coagulation (clot formation) *But all really happen at the same time
67
Vasoconstriction for vessel damage
Happens instantly, local response Vessel releasees vasoconstrictors (seratonin & thromboxane A2) Reduces flow and pressure to wound area, attempting to reduce blood loss
68
Formation of platelet plug
Damaged vessel attracts platelets Platelets stick to the exposed collagen and platelets stick to each other because initially stuck ones release cytokines which activate other platelets (Positive feedback loop)
69
Cytokine
Chemicals released by blood and immune cells
70
Why is platelet plug not enough?
Not strong enough to withstand the shear stress that comes from blood flow pressure
71
Coagulation
formation of fibrin clot over platelet plug 1. damaged cells express tissue factor and collagen which trigger coagulation cascade 2. Divided into intrinsic and extrinsic pathways which converge at common
72
Thrombus
Permanent clot (too strong coagulation response)
73
Embolism
Clot breaks off and gets stuck Pulmonary (capillary bed of lungs) or venous (typically lower legs)
74
Coagulation cascade
Series of enzymatic reactions Once it starts it can't be stopped KNOW WHOLE PATHWAY, slide 33
75
Plasmin
Breaks down fibrin activated by thrombin and tissue plasminogen activator (tPA)
76
Fibrinolysis
the break down of fibrin and thus breakdown of clot
77
4 major functions of respiratory system
1. exchange of gases between atmosphere and blood 2. Homeostatic regulation of blood pH (since CO2 is an acid) 3. Protection from inhaled pathogens and irritating substance (epithelium traps and destroys) 4. Vocalization (air moving across vocal cords)
78
Minor functions of Respiratory system
Water and heat regulation Both released in exhale
79
Bulk flow of Air
Air moves from high to low pressure Muscular pump creates pressure gradients Resistance to air flow is due to diameter of tube
80
External respiration
Movement of gases between environment and cells Exchange between atm and lungs Exchange between lungs and blood Transport of gas into blood Exchange between blood and cells
81
Internal respiration
Cellular respiration: intracellular reactions that use glucose to produce ATP, CO2, and water
82
3 major anatomical components of Respiratory system
Conducting system Alveoli Bones and muscles
83
Conducting system
Passages that lead from external environment to surface of lungs Upper and lower resp. tract NO gas exchange
84
Alveoli
Small, interconnected sacs with their associated pulmonary capillaries that form exchange surfaces Gas exchanged
85
Bones and muscles
Thorax and abdomen; muscular pump
86
Muscles of inspiration
Sternocleidomastoid, scales, external intercostals, diaphragm Pull top of lungs up and bottom down to expand volume
87
Muscles of expiration
Internal intercostals and abdominal muscles
88
Muscles used in quite breathing
NONE! Quiet breathing is passive and does not use muscles, just passive recoil
89
Trend of diameter through lower respiratory tract
Decreases as the air moves down/through
90
Trend of Cross-sectional area through lower respiratory tracts
Increases as air moves down/through Extensive branching
91
Structures with no smooth muscle (cartilage only)
Trachea, primary bronchi, small bronchi, bronchioles
92
Structures with no cartilage (SM only)
Respiratory bronchioles and Alveoli SM allows for change in diameter
93
Pleural sacs
Ensure right and left lungs don't interact Surrounds each lung like a water balloon filled with pleural fluid Reduces friction, holds lungs close to thoracic wall to maximize volume
94
Thorax
Sealed cavity Lungs and heart Three membranous sacs within it (pericardial and R/L pleural)
95
Upper respiratory tract function
Warms air, humidifies air, filters foreign particles
96
Goblet cells
Secrete mucins to help with trapping
97
Epithelial cells
Ciliated (beat and move things along) and secrete Cl- to create saline and loosen mucus
98
Creation of saline
1. NKCC brings Cl- into epithelial cell from ECF (K and Na are transported back out) 2. Apical anion channels like CFTR allow Cl- to enter lumen 3. Na+ goes from ECF to lumen via paracellular pathway moving down the electrochemical gradient 4. NaCl movement from ECF creates CG so water flows into lumen NaCl and water is saline
99
Defective receptor in CF patients
CFTR --> can't properly make saline for mucus, also present in other organs
100
Lower respiratory tract
Exchange of gases Promoted by alveoli cells surrounded by pulmonary capillaries
101
Type 1 Alveoli cells
95%, thin large cells that promote diffusion of gas
102
Type 2 alveoli cells
5%, secrete surfactant and increase compliance of lungs by decreasing surface tension
103
Pulmonary circulation
Blood going to get oxygenated High flow, low pressure (25/8) Receives entire CO of RV
104
Pulmonary hypertension
>25 mmHg leads to RV failure Fatal condition because low pressure system and RV is less muscular
105
Atmospheric pressure
Air exerts a pressure Sea level 760 mmHg (decreases with altitude)
106
Boyle's law
P1V1 = P2V2 As pressure increases, volume decreases
107
Dalton's law
Total pressure exerted by a mixture of gases is the sum of the pressures exerted by the individual gases
108
Partial Pressure (Pgas)
Pressure of a single gas in a mixture Determined by abundance not molecular size Pgas = Patm*(% of gas in atm)
109
Surface tension
Hydrogen bonds of H2O molecules attract one another, so fluid wants to shrink into smallest SA possible
110
Surface tension affect on alveoli
Increases pressure of alveoli because they are covered in fluid and this would oppose gas flow
111
Surfactant
Released by epithelial cells to decrease surface tension Smaller alveoli produce more to equal pressure of larger alveoli to get equal air which means most efficient for overall gas exchange (Law of LaPlace)
112
Resistance of Alveoli
Length and viscosity constant so diameter determines resistance Bronchioles provide most resistance because of SM under neural and hormonal control
113
Neural control of bronchioles
NO SYMP. Para symp fibers --> bronchoconstriction Acts as a reflex
114
Hormonal control of bronchioles
Primarily during high demand Epi- bind B2 receptors of SM and causes bronchodilation ex: Albuterol
115
Paracrine control of bronchioles
Most dominant most the time High CO2 - dilation, relax SM Histamine - constriction, produced by immune cells
116
Allergic reaction
Immune cells produce too much histamine which causes too much constriction
117
Total pulmonary ventilation
TPV = (Ventilation rate)*(tidal volume) Vent. rate is 12-20 breaths per min Tidal V: 500 mL
118
Why does not all air reach alveoli
Anatomical dead space (upper airways have no gas exchange and not all air reaches exchange area) ~150 mL don't make it
119
Alveolar ventilation
Air actually reaching alveoli Alveolar ventilation = (ventilation rate)*(Tidal volume - dead space volume) Short rapid breaths decrease volume that reaches alveoli Long deeper breath increase volume
120
Eupnea
Normal quiet breathing
121
Hyperpnea
Increased resp. rate and/or volume in response to increased metabolism
122
Hyperventilation
Increased resp. rate and/or volume without increased metabolism Increases air to alveoli which leads to low CO2, Increase pH, dizzy/weak/faint/seizure
123
Hypoventilation
Decreased alveolar ventilation shallow breathing, asthma, etc Decrease air leads to low O2 and decrease blood pH More rapid change of PO2 and PCO2
124
Tachypnea
Rapid breathing, increase resp. rate with decreased depth
125
Dyspnea
Difficulty breathing due to pathology or obstruction
126
Apnea
Stop breathing
127
Ventilation-perfusion matching
Lungs match air flow to blood flow in alveoli which promotes efficiency If alveoli receives less air its cap will collapse (High CO2 constricts cap), reversible if alveolar ventilation resumes
128
Uniqueness of pulmonary capillaries
Collapsible: collapse diameter to reduce blood flow Recruitable: recruit dif capillaries based on activity (start at bottom of lungs)
129
PCO2 increase
Dilates bronchioles and systemic arteries (strong) Constricts Pulmonary arteries (weak)
130
PO2 Increase
Constrict bronchioles (weak) and systemic arteries (strong) Dilate pulmonary arteries (stronger) Primarily a PO2 decrease constricts pulmonary arteries
131
Respiratory cycle
One single inspiration followed by a single expiration
132
Tidal Volume
Quiet breathing, at rest Around 500 mL Vt
133
Inspiration reserve volume
Max inhale after quiet exhale Around 3000 mL
134
Expiratory reserve volume
Max exhale after quiet exhale Around 1100 mL
135
Residual volume
Air that remains in lungs after max exhale Prevents alveoli collapse
136
Factors that affect differences in volumes
Gender, age, height, weight, etc
137
Inspiratory capacity
= Vt + IRV See graph
138
Vital capacity
= Vt + IRV + ERV Most physiologically relevant See graph
139
Total lung capacity
= Vt + IRV + ERV + RV See graph
140
Functional residual capacity
= ERV + RV Amount of airs in lungs after quiet exhale See graph
141
What is the pump creating respiratory pressure
Muscles of the thorax Primarily diaphragm
142
Inspiration
Increases volume of thorax Diaphragm drops 60-75% Other muscles pull thorax up 25-40% Active process (muscles contracting, energy used)
143
Expiration
Decrease volume of thorax Muscles relax and recoil thorax Normally a passive process unless exercising
144
Pressure gradients during ventilation
Atm pressure Alveolar (Always greater than intrapleural) Intrapleural Partial pressure of gases in blood Partial pressure of gases in tissues
145
Pneumothorax
Collapsed lung Intrapleural pressure is lower than atm pressure You can survive with a collapsed lung
146
gas that primarily controls bronchioles
CO2 has stronger effect
147
Gas the primarily controls arterioles
O2 has stronger effect
148
What happens when interpleural pressure becomes greater than alveolar?
Air tries to move down its pressure gradient and would collapse the lung. Therefore alveolar pressure must always be greater than interpleural
149
Penetrating chest trauma
Opens interpleural cavity to the atmosphere, air rushes in down its pressure gradient and collapses the lung
150
Compliance
The ability of the lungs to stretch Too high of compliance leads to low elastance
151
Elastance
Elastic recoil, the resistance to stretch Lungs should return to resting volume
152
Emphysema
Disease that destroys the elastin fibers in the lungs, stretch easily but does not recoil to normal volume, so must use muscle to expire
153
PO2 in dry air, alveoli, arterial blood, cells, and venous blood
Dry air: 160 mmHg Alveoli: 100 mmHg Arterial blood: 100 mmHG Cells: < 40 mmHg Venous blood: < 40 mmHg
154
PCO2 in dry air, alveoli, arterial blood, cells, and venous blood
Dry air: 0.25 mmHg Alveoli: 40 mmHg Arterial blood: 40 mmHg Cells: 46 mmHg Venous blood: > 46 mmHg
155
Why does PO2 drop drastically from arterial blood to cell
Because in the cell the O2 is getting used up in the ETC
156
Hypoxia
Low O2
157
Hypercapnia
High CO2
158
3 blood parameters that must be monitored
O2 (aerobic resp.), CO2 (High CO2 depresses CNS), pH (low will denature proteins)
159
Hypoxic hypoxia
Low arterial PO2 Caused by altitude (air comp.), hypoventilation, decreased lung diffusion, abnormal ventilation-perfusion
160
Anemic Hypoxia
Decreased total amount of O2 bound to Hb Caused by blood loss, anemia, Carbon monoxide posion
161
Ischemic hypoxia
Reduced blood flow Caused by heart failure, shock, thrombosis
162
Histotoxic hypoxa
Cells can't use the O2 that is delivered to them Caused by Cyanine or other metabolic poisons
163
Low alveolar PO2 caused by
Composition of inspired air and and alveolar ventilation
164
Composition of inspired air (affecting low alveolar PO2)
Humidity--> high water vapor reduced PO2 Altitude --> PO2 decreases with an increase in altitude because atm pressure decreases. Not because there is less O2 but because there is a smaller pressure gradient for O2 so every breath you take has less O2 in it.
165
Alveolar ventilation affecting low alveolar PO2
Rate and depth of breathing (hypo) Decreased compliance and increased resistance CNS depression
166
Factors affecting gas diffusion between alveoli and blood
Surface area, diffusion distance Fick's law of diffusion, alveolar perfusion (physical block), and other factors like solubility of gas (CO2 more soluble than O2)
167
Surface area affect on alveoli-blood exchange
Total # of alveoli Increase SA, greater exchange Alveloi don't regenerate
168
Diffusion distance affect on alveoli-blood exchange
Increase distance = slower gas exchange Barrier thickness (build up of scar tissue or fibrotic lung disease increase thickness) Amount of fluid (b/w capillary and alveoli). more fluid leads to greater distance Fluid in interstitial space (pulmonary edema)
169
Fick's Law of Diffusion
Diffusion rate proportional to: (SA* CG* Barrier permeability) /distance
170
Mass flow
RATE flow = [O2] * CO Units: [O2] mLO2/L blood CO: L/min Flow: mLO2/min
171
Mass balance
Arterial O2 - venous O2 = oxygen consumption (QO2) Units: mLO2/min Takes into account how much O2 tissues are using
172
Fick's equation
QO2 = CO* (arterial O2 - venous O2)
173
Transport of O2
<2% dissolved in plasma 98% bound to Hb (HbO2) Oxygen obeys mass action (amount in blood = amount going to tissues) Plasma O2 goes to tissues first
174
Hb sponge
At rest tissues only require 250 mLO2/min But at rest at saturation Hb delivers 1000 mLO2/min Hb acts as sponge reservoir of O2 for when demand increases Blood without Hb only has 15 mLO2/min
175
2 factors influence amount of O2 bound to Hb
Partial pressure O2 (PO2) in plasma Number of potential Hb binding sites (decreases with things like Anemia)