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A&P lecture 2 > Exam 2 > Flashcards

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
Q

Absorption

A

Fluid moves into capillary; determined by bulk flow

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26
Q

Filtration

A

Fluid leaves capillary; determined by bulk flow

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27
Q

Hydrostatic pressure (BP)

A

lateral pressure of fluid through pores

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28
Q

Osmotic pressure

A

Determined by solute concentration of fluid; protein concentration in blood –> Colloid osmotic pressure

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29
Q

Fluid movement in capillary

A

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)

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30
Q

Why is colloid osmotic pressure constant from arteriole to venule

A

Because proteins aren’t moving in and out of blood

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31
Q

Lymphatic system

A

Returns the lost fluid back to the blood via emptying into venous system (Vena cava); not a closed loop

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32
Q

Thymus

A

Adaptive immune system, T-cells mature, detect if self or not
Atrophies with age because u are exposed to less new stuff

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33
Q

Spleen

A

Activation site of immune system
Recycle dead RBCs
Reservoir for RBCS
Can live without -> weak immune system

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34
Q

Lymphatic system interaction with other systems

A

CV system- returns fluid lost in capillaries
Digestive- transport of lipids to CV
Immune- recognition and destruction of foreign pathogens

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35
Q

Lymph Vessels

A

Blind ended vessels, lie close to capillaries
Thin flat endothelium
Very porous- protein, cell, bacteria can enter

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36
Q

Larger lymphatic vessels

A

Semilunar valves to prevent backflow, empty into venous subclavian and internal jugular

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37
Q

Lymph nodes

A

Activation of immune system
Fibrous bean nodes
Macrophages and lymphocytes
Antigen recognition

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38
Q

Other structures of lymph system

A

Spleen, thymus, gut-associated lymph tissue

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39
Q

Edema

A

Accumulation of fluid in interstitial space
Inadequate drainage of lymph- protein accumulation in interstitial place
Excessive capillary filtration- increased permeability of caps

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40
Q

Three factors that disrupt capillary filtration

A
  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)
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41
Q

Components of blood

A

Plasma (Fluid)- water, ions, organic molecules, elements, vitamins, gases
Cellular elements (White & red blood cells, platelets)

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42
Q

Plasma

A

ECM
Majority water (92%)
7% protein, 1% dissolved organic substances
Similar to Interstitial fluid but with proteins
Proteins increase osmotic pressure

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43
Q

Plasma proteins

A

Albumin (largest component)
Globulins (antibodies)
Fibrinogen
Transferrin

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44
Q

RBCs

A

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

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45
Q

White blood cells

A

Leukocytes
Only fully functional blood cell
Critical for immune function/defense

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46
Q

5 types of WBCs

A

Lymphocytes, monocytes, neutrophils, eosinophils, basophils

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47
Q

Platelets

A

Thrombocytes
Critical for hemostasis
Lack nucleus
Fragments of megakaryocytes so not a living cell
NSAIDs knock out platelets

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48
Q

Hematopoietic Stem Cell

A

Found in bone marrow (primarily long bones)
Pluripotent- can develop into RBC, WBC, or platelets

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49
Q

Hematopoiesis

A

Synthesis of blood cells
Occurs in embryonic and postnatal environments

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50
Q

Complete Blood count (CBC)

A

Analysis of blood components
Compare blood cell numbers to normal ranges
Indicator of health conditions

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51
Q

Hematocrit

A

Percentage of RBCs in total blood volume
40-54% Males
37-47% Females
Lower in females because of weight/BV

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52
Q

Hemoglobin

A

Oxygen carrying capacity of RBCs
Units: g Hb/dL
14-17 Males
12-16 Females

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53
Q

Red cell count

A

Count of erythrocytes as they stream through beam of light
Units: cells/uL
4.5-6.5E6 Males
3.9-5.6E6 Females

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54
Q

Total white cell count

A

Shoes overall immune response, don’t need to know #s

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55
Q

Shape of RBCs

A

Biconcave disc
Increase SA which increases gas exchange

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56
Q

Erythrocytes (RBCs)

A

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

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57
Q

Hemoglobin (Hb)

A

4 heme groups bind together to create 1 Hb
Major component of RBC

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58
Q

Heme group

A

Binds O2 and CO2
Has 1 iron
Contains 70% of body’s iron
Subunit of Hb

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59
Q

Transferrin

A

Protein that transports iron in the plasma

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60
Q

Ferritin

A

cells’ storage of excess iron, mostly in liver
Extra can be toxic

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61
Q

Iron Transport

A
  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
  7. 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
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62
Q

Hyperbilirubinemia

A

Elevated bilirubin
Jaundice
Infants- fetal Hb accumulation (liver not fully developed)
Adults- liver disease/dysfunc.

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63
Q

Anemia

A

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

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64
Q

Thrombocytes (Platelets)

A

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

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65
Q

Challenges to the repair process

A

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

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66
Q

3 stages of Hemostasis

A

Vasoconstriction
Formation of platelet plug
Coagulation (clot formation)
*But all really happen at the same time

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67
Q

Vasoconstriction for vessel damage

A

Happens instantly, local response
Vessel releasees vasoconstrictors (seratonin & thromboxane A2)
Reduces flow and pressure to wound area, attempting to reduce blood loss

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68
Q

Formation of platelet plug

A

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)

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69
Q

Cytokine

A

Chemicals released by blood and immune cells

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70
Q

Why is platelet plug not enough?

A

Not strong enough to withstand the shear stress that comes from blood flow pressure

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71
Q

Coagulation

A

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
Q

Thrombus

A

Permanent clot (too strong coagulation response)

73
Q

Embolism

A

Clot breaks off and gets stuck
Pulmonary (capillary bed of lungs) or venous (typically lower legs)

74
Q

Coagulation cascade

A

Series of enzymatic reactions
Once it starts it can’t be stopped
KNOW WHOLE PATHWAY, slide 33

75
Q

Plasmin

A

Breaks down fibrin
activated by thrombin and tissue plasminogen activator (tPA)

76
Q

Fibrinolysis

A

the break down of fibrin and thus breakdown of clot

77
Q

4 major functions of respiratory system

A
  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
Q

Minor functions of Respiratory system

A

Water and heat regulation
Both released in exhale

79
Q

Bulk flow of Air

A

Air moves from high to low pressure
Muscular pump creates pressure gradients
Resistance to air flow is due to diameter of tube

80
Q

External respiration

A

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
Q

Internal respiration

A

Cellular respiration: intracellular reactions that use glucose to produce ATP, CO2, and water

82
Q

3 major anatomical components of Respiratory system

A

Conducting system
Alveoli
Bones and muscles

83
Q

Conducting system

A

Passages that lead from external environment to surface of lungs
Upper and lower resp. tract
NO gas exchange

84
Q

Alveoli

A

Small, interconnected sacs with their associated pulmonary capillaries that form exchange surfaces
Gas exchanged

85
Q

Bones and muscles

A

Thorax and abdomen; muscular pump

86
Q

Muscles of inspiration

A

Sternocleidomastoid, scales, external intercostals, diaphragm
Pull top of lungs up and bottom down to expand volume

87
Q

Muscles of expiration

A

Internal intercostals and abdominal muscles

88
Q

Muscles used in quite breathing

A

NONE!
Quiet breathing is passive and does not use muscles, just passive recoil

89
Q

Trend of diameter through lower respiratory tract

A

Decreases as the air moves down/through

90
Q

Trend of Cross-sectional area through lower respiratory tracts

A

Increases as air moves down/through
Extensive branching

91
Q

Structures with no smooth muscle (cartilage only)

A

Trachea, primary bronchi, small bronchi, bronchioles

92
Q

Structures with no cartilage (SM only)

A

Respiratory bronchioles and Alveoli
SM allows for change in diameter

93
Q

Pleural sacs

A

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
Q

Thorax

A

Sealed cavity
Lungs and heart
Three membranous sacs within it (pericardial and R/L pleural)

95
Q

Upper respiratory tract function

A

Warms air, humidifies air, filters foreign particles

96
Q

Goblet cells

A

Secrete mucins to help with trapping

97
Q

Epithelial cells

A

Ciliated (beat and move things along) and secrete Cl- to create saline and loosen mucus

98
Q

Creation of saline

A
  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
Q

Defective receptor in CF patients

A

CFTR –> can’t properly make saline for mucus, also present in other organs

100
Q

Lower respiratory tract

A

Exchange of gases
Promoted by alveoli cells surrounded by pulmonary capillaries

101
Q

Type 1 Alveoli cells

A

95%, thin large cells that promote diffusion of gas

102
Q

Type 2 alveoli cells

A

5%, secrete surfactant and increase compliance of lungs by decreasing surface tension

103
Q

Pulmonary circulation

A

Blood going to get oxygenated
High flow, low pressure (25/8)
Receives entire CO of RV

104
Q

Pulmonary hypertension

A

> 25 mmHg
leads to RV failure
Fatal condition because low pressure system and RV is less muscular

105
Q

Atmospheric pressure

A

Air exerts a pressure
Sea level 760 mmHg (decreases with altitude)

106
Q

Boyle’s law

A

P1V1 = P2V2
As pressure increases, volume decreases

107
Q

Dalton’s law

A

Total pressure exerted by a mixture of gases is the sum of the pressures exerted by the individual gases

108
Q

Partial Pressure (Pgas)

A

Pressure of a single gas in a mixture
Determined by abundance not molecular size
Pgas = Patm*(% of gas in atm)

109
Q

Surface tension

A

Hydrogen bonds of H2O molecules attract one another, so fluid wants to shrink into smallest SA possible

110
Q

Surface tension affect on alveoli

A

Increases pressure of alveoli because they are covered in fluid and this would oppose gas flow

111
Q

Surfactant

A

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
Q

Resistance of Alveoli

A

Length and viscosity constant so diameter determines resistance
Bronchioles provide most resistance because of SM under neural and hormonal control

113
Q

Neural control of bronchioles

A

NO SYMP.
Para symp fibers –> bronchoconstriction
Acts as a reflex

114
Q

Hormonal control of bronchioles

A

Primarily during high demand
Epi- bind B2 receptors of SM and causes bronchodilation
ex: Albuterol

115
Q

Paracrine control of bronchioles

A

Most dominant most the time
High CO2 - dilation, relax SM
Histamine - constriction, produced by immune cells

116
Q

Allergic reaction

A

Immune cells produce too much histamine which causes too much constriction

117
Q

Total pulmonary ventilation

A

TPV = (Ventilation rate)*(tidal volume)
Vent. rate is 12-20 breaths per min
Tidal V: 500 mL

118
Q

Why does not all air reach alveoli

A

Anatomical dead space (upper airways have no gas exchange and not all air reaches exchange area)
~150 mL don’t make it

119
Q

Alveolar ventilation

A

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
Q

Eupnea

A

Normal quiet breathing

121
Q

Hyperpnea

A

Increased resp. rate and/or volume in response to increased metabolism

122
Q

Hyperventilation

A

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
Q

Hypoventilation

A

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
Q

Tachypnea

A

Rapid breathing, increase resp. rate with decreased depth

125
Q

Dyspnea

A

Difficulty breathing due to pathology or obstruction

126
Q

Apnea

A

Stop breathing

127
Q

Ventilation-perfusion matching

A

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
Q

Uniqueness of pulmonary capillaries

A

Collapsible: collapse diameter to reduce blood flow
Recruitable: recruit dif capillaries based on activity (start at bottom of lungs)

129
Q

PCO2 increase

A

Dilates bronchioles and systemic arteries (strong)
Constricts Pulmonary arteries (weak)

130
Q

PO2 Increase

A

Constrict bronchioles (weak) and systemic arteries (strong)
Dilate pulmonary arteries (stronger)
Primarily a PO2 decrease constricts pulmonary arteries

131
Q

Respiratory cycle

A

One single inspiration followed by a single expiration

132
Q

Tidal Volume

A

Quiet breathing, at rest
Around 500 mL
Vt

133
Q

Inspiration reserve volume

A

Max inhale after quiet exhale
Around 3000 mL

134
Q

Expiratory reserve volume

A

Max exhale after quiet exhale
Around 1100 mL

135
Q

Residual volume

A

Air that remains in lungs after max exhale
Prevents alveoli collapse

136
Q

Factors that affect differences in volumes

A

Gender, age, height, weight, etc

137
Q

Inspiratory capacity

A

= Vt + IRV
See graph

138
Q

Vital capacity

A

= Vt + IRV + ERV
Most physiologically relevant
See graph

139
Q

Total lung capacity

A

= Vt + IRV + ERV + RV
See graph

140
Q

Functional residual capacity

A

= ERV + RV
Amount of airs in lungs after quiet exhale
See graph

141
Q

What is the pump creating respiratory pressure

A

Muscles of the thorax
Primarily diaphragm

142
Q

Inspiration

A

Increases volume of thorax
Diaphragm drops 60-75%
Other muscles pull thorax up 25-40%
Active process (muscles contracting, energy used)

143
Q

Expiration

A

Decrease volume of thorax
Muscles relax and recoil thorax
Normally a passive process unless exercising

144
Q

Pressure gradients during ventilation

A

Atm pressure
Alveolar (Always greater than intrapleural)
Intrapleural
Partial pressure of gases in blood
Partial pressure of gases in tissues

145
Q

Pneumothorax

A

Collapsed lung
Intrapleural pressure is lower than atm pressure
You can survive with a collapsed lung

146
Q

gas that primarily controls bronchioles

A

CO2 has stronger effect

147
Q

Gas the primarily controls arterioles

A

O2 has stronger effect

148
Q

What happens when interpleural pressure becomes greater than alveolar?

A

Air tries to move down its pressure gradient and would collapse the lung. Therefore alveolar pressure must always be greater than interpleural

149
Q

Penetrating chest trauma

A

Opens interpleural cavity to the atmosphere, air rushes in down its pressure gradient and collapses the lung

150
Q

Compliance

A

The ability of the lungs to stretch
Too high of compliance leads to low elastance

151
Q

Elastance

A

Elastic recoil, the resistance to stretch
Lungs should return to resting volume

152
Q

Emphysema

A

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
Q

PO2 in dry air, alveoli, arterial blood, cells, and venous blood

A

Dry air: 160 mmHg
Alveoli: 100 mmHg
Arterial blood: 100 mmHG
Cells: < 40 mmHg
Venous blood: < 40 mmHg

154
Q

PCO2 in dry air, alveoli, arterial blood, cells, and venous blood

A

Dry air: 0.25 mmHg
Alveoli: 40 mmHg
Arterial blood: 40 mmHg
Cells: 46 mmHg
Venous blood: > 46 mmHg

155
Q

Why does PO2 drop drastically from arterial blood to cell

A

Because in the cell the O2 is getting used up in the ETC

156
Q

Hypoxia

A

Low O2

157
Q

Hypercapnia

A

High CO2

158
Q

3 blood parameters that must be monitored

A

O2 (aerobic resp.), CO2 (High CO2 depresses CNS), pH (low will denature proteins)

159
Q

Hypoxic hypoxia

A

Low arterial PO2
Caused by altitude (air comp.), hypoventilation, decreased lung diffusion, abnormal ventilation-perfusion

160
Q

Anemic Hypoxia

A

Decreased total amount of O2 bound to Hb
Caused by blood loss, anemia, Carbon monoxide posion

161
Q

Ischemic hypoxia

A

Reduced blood flow
Caused by heart failure, shock, thrombosis

162
Q

Histotoxic hypoxa

A

Cells can’t use the O2 that is delivered to them
Caused by Cyanine or other metabolic poisons

163
Q

Low alveolar PO2 caused by

A

Composition of inspired air and and alveolar ventilation

164
Q

Composition of inspired air (affecting low alveolar PO2)

A

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
Q

Alveolar ventilation affecting low alveolar PO2

A

Rate and depth of breathing (hypo)
Decreased compliance and increased resistance
CNS depression

166
Q

Factors affecting gas diffusion between alveoli and blood

A

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
Q

Surface area affect on alveoli-blood exchange

A

Total # of alveoli
Increase SA, greater exchange
Alveloi don’t regenerate

168
Q

Diffusion distance affect on alveoli-blood exchange

A

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
Q

Fick’s Law of Diffusion

A

Diffusion rate proportional to:
(SA* CG* Barrier permeability) /distance

170
Q

Mass flow

A

RATE
flow = [O2] * CO
Units: [O2] mLO2/L blood
CO: L/min
Flow: mLO2/min

171
Q

Mass balance

A

Arterial O2 - venous O2 = oxygen consumption (QO2)
Units: mLO2/min
Takes into account how much O2 tissues are using

172
Q

Fick’s equation

A

QO2 = CO* (arterial O2 - venous O2)

173
Q

Transport of O2

A

<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
Q

Hb sponge

A

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
Q

2 factors influence amount of O2 bound to Hb

A

Partial pressure O2 (PO2) in plasma
Number of potential Hb binding sites (decreases with things like Anemia)

A&P lecture 2 (4 decks)

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