BHS 116 – Physiology
Notetaker: Jenna Rogers
Date: 10/21/2011, 1st
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Review for Final Exam: New Material (not all inclusive)
RESPIRATORY
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Ventilation- expiration and inspiration and how the muscles work
Boyle’s law- physics of inspiration and expiration
o Changes in V of thoracic cavity and P changes in the alveoli that accompany the V
change
Alveolar surface tension
o They want to collapse due to:
 Elasticity
 Surface tension by water molecules causes the smaller alveoli to want to
collapse into the larger ones
 Surfactant reduces surface tension- secreted by type II pneumocytes
2 types of ventilation
o Pulmonary ventilation- total taken in per minute
 Includes dead space volume- no exchange with blood
o Alveolar ventilation- air that makes it into the alveoli, capable of gas exchange
o Alveolar is always lower than the pulmonary (have to subtract out the dead space)
Respiratory membrane- alveolar and capillary membranes
o Factors that effect gas diffusion rate- know they change
 Ex. Change in the gradient
Ventilation Perfusion ratio
o Regions of the lung where there are different rates of ventilation and perfusion (blood
flow)
o Ideal: 1 to 1
o Top of lung- ventilation > perfusion DEAD SPACE
 Pathology- vascular obstruction
o Bottom of lung- perfusion > ventilation SHUNT
 Pathology- airway obstruction
Local Controls of Ventilation- Perfusion Ratio- alter states of constriction and dilation
o Understand the normal regulation
o Vascular and bronchiole vasoconstriction and dilation to normalize ventilation and
perfusion
Gas transport in Blood
o Different btwn O2 and CO2
o O2 carried by hemoglobin – 98%
 Other is physically dissolved- the only factor contributing to PO2
o CO2 carried as Bicarbonate
 Taken up by RBC and converted to bicarbonate
 Can also be bound to hemoglobin
Oxygen- hemoglobin dissociation curve
BHS 116 – Physiology
Notetaker: Jenna Rogers
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At different PO2- what is the saturation state of the hemoglobin
 Normal in Arteriole PO2 of 100% (what it is in the alveoli)
 Tissue- PO2= 40. Tissues use up oxygen and is lower in the venous system
 As O2 is delivered to tissues- we give up 25% of bound O2 to tissues
 Hemoglobin still saturated= tremendous O2 reserves
 When PO2 is less than 40 (exercise) there is a stronger and faster delivery of O2
to the tissues
o Bohr effect- factors influence the dissociation of O2 from hemoglobin (PCO2 and PH)
 Tissues:
 PCO2- as blood is delivered to tissues, PO2 is lower but PCO2 is elevated
 Elevated PCO2 lowers the ph at the tissues lever
 Increased PCO2 and decreased PH shifts curve to the right
 Lungs
 lower PCO2 and higher PO2 so the curve shifts back to left
 temperature can also shift curve- not part of bohr effect
 elevated temp shifts it to the right
Haldane effect
o Tissue- elevated PCO2 and decreased PO2 drives O2 off hemoglobin
 CO2 and H can bind to hemoglobin much easier
Summary of Transport of gas molecules at level of tissues and alveoli
o Oxygen is bound to hemoglobin or freely dissolved in blood
o CO2 is bound to hemoglobin, freely dissolved in blood or is converted to bicarbonate
Control of Respiration
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Dorsal Respiratory Group (DRG)- only inspiratory neurons
o Trigger contraction of diaphragm= inspiration
o Stop firing= relaxation and expiration
Ventral Respiratory Group- inspiratory and expiratory neurons
o More active ventilation
Apneustic center- prevents pneumotastic center from switching on
o Acts against pneumotaxic
o Encourages extreme periods of inspiration
Pneumotastic center- switch off DRG to get expiration
Pre-Botzinger complex= pacemaker
Chemoreceptors- sense concentration of CO2 and O2 in blood
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Date: 10/21/2011, 1st
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Peripheral- monitors PO2 changes when <60 mm HG
o Weakly responds to increased changes in PCO2 and H
o Low O2 levels inhibits respiratory center
BHS 116 – Physiology
Notetaker: Jenna Rogers
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Peripheral chemoreceptors are an emergency resort to stimulates medullary respiratory
center to increase respiration
Central
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Primary driver of respiration for minute to minute breathing
Sensitive to CO2 changes
Increased PCO2= Increaed ventilation rate to blow off excess CO2
Primary mechanism
 CO2 diffuses in blood brain barrier, combines with water to form carbonic acid,
dissociates into H ions and bicarbonate
 H ions bind to receptors and stimulate respiratory center
Bicarbonate Buffering System
o First defense against changes in blood ph
o Decrease in PH drives curve to left- increase in CO2 which is expired by the lungs
o Increase in PH drives curve to the right- decreases CO2, more HCO3 made which is
excreted in the urine
Alveolar ventilation effects PH
o Increase ventilation= decrease in PCO2, decrease carbonic acid levels, lowers H ions,
increases PH
o Decrease ventilation= increase PCO2, increase carbonic acid levels, higher H ions,
decreases PH
PH changes in the blood effect the ventilation rate
o Decrease PH of blood, increases ventilation, increases H shifts curve to Left
o Increase PH of blood decreases ventilation to build up CO2, decreases H shifts curve to
Right
Effects of hydrostatic pressure gradient on Pulmonary circulation
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Zone 1- only in pathological condision
o Alveolar pressure > BP= collapsed
Zone 2- upper lung
o Systole= BP > alveolar = open vessel
o Diastole= BP< alveolar – closed vessel
Zone 3- majority of lung
o BP always > alveolar= always open vessel
Exercise- upper lung is converted from zone 2 to 3
Pathologies
COPD- all diseases where there is a problem of expiration
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Date: 10/21/2011, 1st
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Increased RV- air can’t be expired and continues to build up
Increased TLC- exceeds normal lung capacity
BHS 116 – Physiology
Notetaker: Jenna Rogers
Date: 10/21/2011, 1st
Page4
Emphysema- disease of alveoli
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Centriacinaro Most common- chronic smokers
o Effects respiratory bronchiole (not terminal alveoli)
Panacinar
o Rare- more in genetic deficiency of alpha 1-antitrypsin
o Effects entire acinus
Forced Expiratory Vital Capacity
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Ratio= FEV1/FEC
o Normal= 80% expiration of air in 1st sec
o COPD= below 50% problems expiring
Pathogenesis
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Smoking
o Antioxidant/ oxidant imbalance
o Protease/antiprotease imbalance
Asthma
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Intrinsic
o Not an immune reaction
o Triggered by virus
o Same as extrinsic but NO IgE
Extrinsic
o Allergic reaction
o Become hypersentitized to allergen
 Breath in again, mast cells activated= histamine= problems
 Edema and excessive mucus secretion
 Bronchoconstriction
 Increased IgE
 Immediate and chronic/late phase
 Eosinophils
Bronchiole wall changes
o Increased basement membrane thickness, lamina propria thickness increases, smooth
muscle layer increase, increase in activity of goblet cells, elevated eosinophils
Chronic Bronchitis
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Hypersecretion of mucus
Hypertrophy of mucus glands
BHS 116 – Physiology
Notetaker: Jenna Rogers
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Date: 10/21/2011, 1st
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Smoking- persistant irritation = inflammation= narrows bronchiole airways
Longs time= fibrosis which becomes irreversible damage
CHRONIC RESTRICTIVE LUNG DISEASE
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Disease of inspiration
o Reduced compliance
Decrease in TLC- can’t bring as much air in
RV= normal
Decrease in VC
Unchanged ratio of FEV1/FVC
o Unlike obstruction
IPF
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Injury to alveolar wall= damage= inflammation
Injury removed= ok
Persistent= fibrosis- irreversible which effects the diffusion of gas between blood and alveoli
Activation of macrophages
o Activate neutrofils, stimulate fibroblasts (lay down fibrosis proteins)
Hypersensitivity Pneumonitis (hypersensitivity= allergy)
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Stimulates the immune system= allergic alveolitis
Damage at the level of the alveoli (similar to asthma Sx)
Diffuse Alveolar Hemorrhage Syndrome
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Immune system is attacking the lungs
Pulmonary basement membrane- effects alveolar wall and capillary way
Blood enters alveoli
Hemotisis and anemia
Pulmonary Thromboembolism
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Large blot clots moving from lower leg veins to pulmonary
2 consequences
o Increase in pulmonary arterial pressure- pulmonary hypertension and thickening of right
ventricular wall
o Ischemia to downstream lung tissues= nonfunctional
Secondary Pulmonary Hypertension
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Result of another disorder
o COPD- emphysema
BHS 116 – Physiology
Notetaker: Jenna Rogers
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Date: 10/21/2011, 1st
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Thromboemboli- blocks blood flow and heart has to work harder to push against
blockage
Left to right shunt heart disease- pumping out extra volume and builds up pressure in
pulmonary
Primary Pulmonary Hypertension
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Genetic- mutation in BMPR2 gene
Normal: decreases pulmonary smooth muscle proliferation
Mutated: not present and smooth muscle proliferates
o Vessel wall thickens and lumen narrows= decrease in blood flow
INFECTIOUS DISEASES
TB
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Microbacteria affects alveolar macrophages
Mechanisms to prevents its own destruction= proliferation of bacteria
Macrophages activate helper T
o Stimulate macrophages to kill off bacteria by releasing nitrous oxide
o More immune cells herd infected macrophages and wall them off= GRANULOMA
 Prevents further spread of bacteria
Primary TB- Initial exposure
o Granuloma formation but asymptomatic
o Can remain latent
o Reactivated= massive immune response
Secondary TB- reactivated
o Destroys upper lobes of lung- immune response starts destroying normal tissues
o Miliary TB= systemic
 Spleen and liver granulomas formed
Primary and Secondary Ocular TB
Pneumonia- any infection of the lung
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Bronchopneumonia
Lobar- common
o Alveoli fill up with edema, neutrophils, RBC
 Decrease respiratory alveolar area- no room for air
o 4 stages
 Congestion
 Red Hepadization
 Gray Hepadization
 Resolution
BHS 116 – Physiology
Notetaker: Jenna Rogers
Date: 10/21/2011, 1st
Page7
GENETIC DISEASES
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Know difference between hereditary and congenital
Know main differences between types of disorders (autosomal dominant, recessive etc)
Autosomal Dominant- protein structure
1.Marfans Syndrome
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Fibrillin 1
3 sites: (know specifics)
o skeleton
o eye
o CV system
2. Familial Hypercholesterolemia- mutation in LDL receptor
Recessive Disorders- involve enzymes
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Need both copies of mutant gene
Carrier- 1 copy
1.Glycogen Storage Diseases- defects in glycogen synthesis- can’t make glucose from glycogen
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Hepatic form- liver
o Glycogen builds up but can’t be broken down
o Hypoglycemia
Myopathic form- skeletal
o Cramping early in exercise- unable to break down glycogen to glucose for ATP
Cystic Fibrosis- epithelial transport disease
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Effects exocrine gland
High levels of NaCL in seat- higher amount in sweat, the more severe the disorder
Mutation in CFTR gene- cAMP dependent chloride channel protein
o Deletion mutation
Channel functions in different tissue types:
Tissue type
normal
mutated
Seat duct
Allows Cl into epithelium
Increase in NaCl in sweat
Air ways
Allows Cl to leave cells and
Thick mucus produced
enter mucus
X- Linked Disorders
BHS 116 – Physiology
Notetaker: Jenna Rogers
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Date: 10/21/2011, 1st
Page8
Afflicted males do not pass onto sons (only daughters)
Know genetic crosses
Hemophilia- factor VIII mutation
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Severe bleeding in normal injury
Spontaneous bleeding into joints= hemarthroses= arthritic condition
Fragile X
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Trinucleotide repeat (like huntington’s disease)
Targets FNR1 gene
o Unable to transport mRNA to distal sites in neurons- synapses not formed
 high level of mental retardation
Can have a permutation
o Male has premutation= normal
o Passes premutation onto all daughters
o Daughter can transmit as a full mutation if changes occur during oogenesis
o Can now pass full mutation onto male offspring= affected
Chromosomes
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Normal Karyotype
Polyploidy- extra sets
Aneuploidy- extra single chromosome
o Trisomy 21 caused by nondisjunction (error in meiosis)
Different Mutations
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Point mutation
Frame shift
Trinucleotide repeat
Chromosome structure abnormalities