Escolar Documentos
Profissional Documentos
Cultura Documentos
Prepared by
DENNIS N. MUÑOZ, PT, RN,RM
Organs of the Respiratory system
•Nose
•Pharynx
•Larynx
•Trachea
•Bronchi
•Lungs –
alveoli
SLIDE 13.2
The Nose
Figure 13.2
SLIDE
13.3B
Anatomy of the Nasal Cavity
SLIDE
13.4A
Upper Respiratory Tract
Olfactory epithelium
Figure 13.2
SLIDE
13.3B
Anatomy of the Nasal Cavity
SLIDE
13.4B
Anatomy of the Nasal Cavity
SLIDE
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
13.4B
Upper Respiratory Tract
Figure 13.2
SLIDE
13.3B
Paranasal Sinuses
SLIDE
13.5B
THE PARANASAL SINUSES
SLIDE 13.6
Pharynx (Throat) SLIDE 13.6
•Nasopharynx is only
respiratory
•The oropharynx and
laryngopharynx
•Common
passageways for
air and food
•Part of two body
systems
SLIDE 13.7
Upper Respiratory Tract
Figure 13.2
SLIDE
13.3B
Larynx (Voice Box)
SLIDE 13.8
ANATOMY OF THE LARYNX
Figure 21.5a, b
Structures of the Larynx
•Thyroid cartilage
•Largest hyaline cartilage
•Protrudes anteriorly (Adam’s apple)
•Epiglottis
•Superior opening of the larynx
•Protects larynx during swallowing
SLIDE
13.9A
Structures of the Larynx
SLIDE
13.9B
MOVEMENTS OF THE VOCAL FOLDS
Figure 21.6
Trachea (Windpipe)
SLIDE
13.10
THE TRACHEA
Figure 21.7a
Primary Bronchi
SLIDE
13.11
BRONCHIAL (RESPIRATORY) TREE
Figure 21.8a
Lungs
SLIDE
13.12A
STRUCTURE OF THE LUNGS
Figure 21.8a
Coverings of the Lungs
SLIDE
13.13
Pleural Membranes and Cavity
Figure 13.4b
SLIDE
13.12B
Respiratory Tree Divisions
SLIDE
13.14
BRONCHIAL (RESPIRATORY) TREE
Figure 21.8a
Bronchioles
•Smallest
branches
of the
bronchi
Figure 13.5a
SLIDE
13.15A
Bronchioles
•All but the
smallest
branches
have
reinforcing
cartilage
Figure 13.5a
SLIDE
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
13.15B
Bronchioles
•Terminal
bronchioles
end in
alveoli
Figure 13.5a
SLIDE
13.15C
Respiratory ZoneRegion of gas
exchange between
air and blood.
•Structures
•Respiratory
bronchioles
•Alveolar duct
•Alveoli
•The Site of gas
exchange
SLIDE
13.16
Alveoli
•Structure of alveoli
•Alveolar duct
•Alveolar sac
•Alveolus
•Gas exchange:
•takes place in the alveoli
•across the respiratory membrane
ALVEOLI
is 1 cell layer thick.
Total air barrier is 2
cells across (2 µ m).
alveoli is reduced.
As alveoli radius decreases,
RDS.
ARDS.
Respiratory Membrane
(Air-Blood Barrier)
SLIDE
13.18A
Respiratory Membrane
(Air-Blood Barrier)
Figure 13.6
SLIDE
13.18B
Gas Exchange
SLIDE
13.19
Events of
Respiration
•Pulmonary ventilation
– moving air in and
out of the lungs
•External respiration –
gas exchange
between pulmonary
blood and alveoli
Events of Respiration
SLIDE
13.20B
Mechanics of Breathing
(Pulmonary Ventilation)
Ventilation
•Completely mechanical
process
•Depends on volume
changes in the thoracic
cavity
•Volume changes lead to
pressure changes, which
lead to the flow of gases
to equalize pressure
Mechanics of
Breathing
(Pulmonary
Ventilation)
•Two phases
•Inspiration – flow of
air into lung
•Expiration – air
leaving lung
Contraction of diaphragm,
increases thoracic volume
vertically.
Parasternal and external
intercostals contract, raising
the ribs; increasing thoracic
volume laterally.
Pressure changes:
Figure 13.7a
SLIDE
13.22B
Expiration
•A passive process
•depends on natural lung elasticity
•As muscles relax, air is pushed out of the
lungs
•Forced expiration can occur by contracting
internal intercostal muscles
SLIDE
13.23A
Quiet expiration is a passive
process.
After being stretched by
EXPIRATION
contractions of the diaphragm
and thoracic muscles; the
diaphragm, thoracic muscles,
thorax, and lungs recoil.
Decrease in lung volume raises
the pressure within alveoli
above atmosphere, and
pushes air out.
Pressure changes:
Intrapulmonary pressure
changes from –3 to +3 mm
Hg.
Intrapleural pressure changes
from –6 to –3 mm Hg.
Transpulmonary pressure = +6
mm Hg.
Expiration
Figure 13.7b
SLIDE
13.23B
Nonrespiratory Air Movements
•Can be caused by reflexes or voluntary
actions
•Examples
•Cough and sneeze – clear lungs of
debris
•Laughing
•Crying
•Yawn
•Hiccup
SLIDE
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
13.25
PULMONARY VENTILATION
Capacities
SLIDE
13.26
Respiratory Volumes and
Capacities
•Inspiratory reserve volume (IRV)
•Amount of air that can be taken in
forcibly over the tidal volume
•Usually between 2100 and 3200 ml
SLIDE
13.27A
Respiratory Volumes and
Capacities
•Expiratory reserve volume (ERV)
•Amount of air that can be forcibly
exhaled
•Approximately 1200 ml
SLIDE
13.27A
Respiratory Volumes and
Capacities
•Residual volume
•Air remaining in lung after expiration
•About 1200 ml
SLIDE
13.27B
Respiratory Volumes and
Capacities
•Vital capacity
•The total amount of exchangeable air
•Vital capacity = TV + IRV + ERV
•Dead air space or volume
•Air that remains in conducting zone
•Bronchi, bronchioles, ducts
•never reaches alveoli
•About 150 ml
SLIDE
Copyright © 2003 Pearson Education, Inc. publishing as Benjmin Cummings
13.28
Respiratory Volumes and
Capacities
•Functional volume
•Air that actually reaches the respiratory
zone
•Usually about 350 ml
•Respiratory capacities are measured
with a spirometer
Respiratory Volumes and
Capacities
•Factors that affect respiratory capacity
•Size
•Sex
•Age
•Physical condition
•
Respiratory Capacities
Figure 13.9
Gas Transport in the Blood
Figure 13.11
SLIDE
13.34B
PARTIAL PRESSURES OF
GASES IN BLOOD
When a liquid or gas (blood
and alveolar air) are at
equilibrium:
The amount of gas
dissolved in fluid
reaches a maximum
value (Henry’s Law).
Depends upon:
Solubility of gas in the
fluid.
Temperature of the fluid.
Partial pressure of the gas.
[Gas] dissolved in a fluid
depends directly on its
partial pressure in the gas
mixture.
SIGNIFICANCE OF BLOOD P0 AND 2
PC0 MEASUREMENTS
2
• At normal P0 2
arterial
blood is
about 100
mm Hg.
• P02 level in the
systemic
veins is
about 40
mm Hg.
Medulla.
Peripheral:
VENTILATION
Throughout Life
•Newborns: 40 to 80 respirations per
minute
•Infants: 30 respirations per minute
•Age 5: 25 respirations per minute
•Adults: 12 to 18 respirations per minute
•Rate often increases somewhat with old
age
SLIDE
13.49
Respiratory Rate Changes
Throughout Life
•Newborns: 40 to 80 respirations per
minute
•Infants: 30 respirations per minute
•Age 5: 25 respirations per minute
•Adults: 12 to 18 respirations per minute
•Rate often increases somewhat with old
age
SLIDE
13.49
Respiratory Disorders: Chronic
SLIDE
13.40A
Emphysema: FYI
SLIDE
13.41
Chronic Bronchitis: FYI
•Mucosa of the lower respiratory
passages becomes severely inflamed
•Mucus production increases
•Pooled mucus impairs ventilation and
gas exchange
•Risk of lung infection increases
•Pneumonia is common
•Hypoxia and cyanosis occur early
SLIDE
13.42
Lung Cancer: FYI
SLIDE
13.44
Sudden Infant Death syndrome
(SIDS): FYI
SLIDE
13.45
Asthma: FYI
SLIDE
13.46
Birth Defects of the Respiratory
System: FYI
•Important birth defects
•Cystic fibrosis
•Common genetic condition
•Over-secretion of thick mucus clogs
the respiratory system
•Cleft palate: developmental anomaly
SLIDE
13.47B
Aging Effects: FYI
•Elasticity of lungs decreases
•Vital capacity decreases
•Blood oxygen levels decrease
•Stimulating effects of carbon dioxide
decreases
•More risks of respiratory tract infection
•New evidence that in estrogen may
be related to COPD
SLIDE
13.48
Pulmonary Physical
Examination and Health
Assessment
Prepared by
• Level of consciousness
– Oriented to person, time & place (x3)
– Obtunded? Lethargic? Confused?
Inspecting the Patient
• Vital Signs
– Temperature - Febrile? Hypothermic?
– Pulse - Tachycardia? Irregular? Faint?
Pulsus paradoxicus? Pulsus alterans
– Respiration- Tachypnea? Shallow?
Deep?
– Blood pressure- Hypotensive?
Hypertensive? Syncope?
Inspecting the Patient
• Examination of Head
– Nasal Flaring
– Cyanosis
– Pursed lip breathing
– Look of anxiety
• Examination of Neck
– Trachea: midline?
– Jugular veins distended?
Examination of the Thorax & Lungs
• Thoracic configuration:
• Barrel chest?
• Kyphosis
• Scoliosis?
• Kyphoscoliosis?
• Pectus excavatum
• Breathing Pattern & Effort
• Retractions? intercostal; supraclavicular
Breathing Pattern & Effort continued
• Synchrony of diaphragm & upper chest?
– Diaphragm & upper chest should work
together
– Abdominal paradox - upper chest rises
while diaphragm falls
• This indicates fatigue of the diaphragm
• Is a excellent predictor of impending
“respiratory failure”
Palpation
• The art of touching the chest wall to
evaluate underlying structures
Aspects of Palpation
• Skin & subcutaneous tissues
– evidence of subcutaneous emphysema?
• Aka - crepitus
– pain associated with bruising &/or rib
fractures?
• Vocal fremitus
• Thoracic expansion
Percussion of the Chest
• Act of tapping on the chest wall (rib
interspaces) to evaluate underlying
structures
– Percussion Sounds:
• Dull - indicates fluid or increased tissue
density
• Hyperressonant (hollow sound) - indicates
increased air- (heard above a
pneumothorax)
Auscultation of the Lungs
• Listening to body sounds with stethescope
Auscultation
• Listening to breath sounds
– Stethoscope
• Bell - for low pitched sounds (heart
sounds)
• Diaphragm - for higher pitched sounds
(breath sounds)
– Technique
• Patient breathes through their mouth
• Ideally, sounds on one side of the chest
should be compared to the opposite side
• May be necessary to have patient roll patient
side-to-side
Normal Breath Sounds
• Vesicular sounds
– Soft “rustling” sounds heard over most lung tissue
• Bronchovesicular sounds
– Has characteristics of above two
– Heard only over major airways
• Tracheal sounds
– Hollow tubular sounds
–
Abnormal (Adventitious) Breath
Sounds
• Crackles (rales)
– discontinuous ”pop-like” sounds
• generally heard on inspiration but can be
heard on exhalation also
• Wheezes
– high-pitched continuous musical sounds
• can be heard on both inspiration or
exhalation
•
Abnormal Breath Sounds Continued
• Rhonchi
– low-pitched snoring sound that is
continuous
• can be heard on inspiration or exhalation
• Bronchial Breath Sounds
– same as Tracheal Sounds except heard
over lung parenchyma
Abnormal Breath Sounds Continued
• Stridor - high pitched raspy sound
– is heard at it’s loudest over the trachea
–
– indicates upper airway narrowing
– heard in such conditions as;
• post extubation stenosis
• croup in young children
Abnormal Breath Sounds Continued
• Pleural Friction Rub
• Egophony - e to a changes
– first section heard is the normal e sound
– second sound heard is the example of
egophony: letter “e” heard as “a”
Crackles can indicate
• Atelectasis
• Bronchitis
• Pneumonia
• Pulmonary edema
• Pulmonary fibrosis (dry crackles)
Ronchi indicates
• Secretions in larger airways
– frequently clear with a cough
– seen in any condition that creates lung
mucus
– in COPD ronchi may occur because of
airflow obstruction unrelated to
secretions
Other “Less Common” Sounds
• Pleural friction rub
– occurs when pleural surfaces rub together
– seen in some pneumonias effecting pleural
surfaces
• Stridor
– High pitched rasping sound heard mainly
on inspiration
– Indicative of upper airway obstruction
Breathing Patterns
• Cheyne-Stokes Breathing
– Irregular patterns of deep breathing followed by
periods of shallow breathing; usually ending with
a period of apnea
• Biot’s Breathing
– Irregular patterns of breathing; usually very
disorganzied. May be periods of apnea
• Kussmaul’s Breathing
– Rapid & deep breathing
More Breathing Patterns
• Apneustic Pattern
– Prolonged inspirations; serial inspirations w/o
exhalation after each followed by “summative”
exhalation
• Asthmatic Pattern
– Excessively long expiratory periods
• Paradoxical Breathing
– Is present when a portion of chest wall moves in
the opposite direction as it should during the
breathing cycle
Voice Sounds
• Egophony
1. Place stethoscope over lung area
2. Ask patient to say the letter “e”
3. If you actually hear the hard “a” sound;
4. The area has a fluid or consolidation
• Bronchophony
– An increase in intensity and clarity of
vocal sounds.
Cardiac Sounds
• Lub - Dub
• S1, S2
• PMI (Point of Maximal Impulse)
– Fifth intercostal, mid clavicular, left side
• PVC’s are common
• Heaves, gallops, murmurs, bruits
Abdominal Examination
• Is the abdomen distended?
• Is the abdomen hard when palpating it?
• Increased abdominal pressure can put increased
pressure on the diaphragm making breathing
more difficult. Causes
– Hepatomegaly
– Intra-abdominal bleeding
Examination of the Extremities
• Look for evidence of
– Cyanosis
• hands, feet, mucous membranes
– Pedal edema (pitting edema)
• +1 to +5 scale used
– Clubbing of fingers
• seen in a variety of inflammatory diseases
– Capillary refill
– Peripheral skin temperature
Clubbing illustrated
Respiratory Assessment
The xiphoid
The Manubrium
• Anterior Chest
• Midsternal Line
• Midclavicular Line- bisects the center of
each clavicle at point halfway between
the palpated sternoclavicular and
acromioclavicular joint, near nipple
line
• Posterior Chest
• vertebral Line- midspinal
• Scapular line- extends through inferior
angle of scapula
• Lateral Chest- Lift arms 90* & divide by 3
lines
• Anterior axillary- down from anterior
axillary fold to where the pectoralis
major muscle inserts
• Posterior anillary down from posterior
axillary fold to where latissimus dorsi
muscle inserts
• Midaxillary line-down from apex of
axilla, lies between and parallel to
other two
• Thoracic cavity
– Mediastinum- middle section of thoracic
cavity contains esophagus, trachea,
heart and great vessels; and the Left
& Right pleural cavities
– Lung Borders- anterior
• Apex 9 highest point of lungs 3-4
cm above inner 3rd of clavicles
• Base- lower border, rest on
diaphragm about 6th rib in
midclavicular line
•
-
–
–
• Anterior Left Upper Lobe (LUL)
• Anterior Left Lower Lobe (LLL)
• Posterior
– Right Upper Lobe (RUL) and Left Upper
Lobe (LUL)- from apices at T1 down to
T3
– Right Lower Lobe (RLL) and Left Lower
Lobe (LLL)- from the above border to
T10 on expiration and to T12 on
inspiration.
•
• Pleurae- thin slippery which forms an
envelope between lungs and chest wall.
• Visceral Pleura- lines outside of lungs down
into fissures
• Parietal Pleura- lining inside the chest
wall and diaphragm.
Objective
A.Inspection (what you see)
1.Shape and Configuration of chest
wall.
a.Thorax symmetric, elliptical
shape with downward
sloping ribs
b.Any signs tumors, lumps,
bruising on chest
–Check shape for:
»Scoliosis (“s” shape)
»Kyphosis (humpback)
»Barrel chest
»
Skin color and condition
»Person’s position
»Level of consciousness
(LOC)
B. Palpation
C Percuss
client’s skin
–
Avoid striking client’s ribs & scapulae,
always a dull sound & yields no data
Lung Field
• Start at apices at top of both
shoulders
• Percuss interspaces comparing
side to side going down lung
region
–Hyperresonance- too much
air present
–Resonance-voice heard
through stethoscope; is
muffled nondistinct
-Dull- abnormal density in lung
h Listening to own breathing
Stethoscope tubing bumping
Patient shivering
Patient has hairy chest
Rustling of paper gown
Music or talking in background
i. Normal breathing Sounds- for adults
a.Bronchial (tracheal) –loud, high
pitched, over trachea and larynx
b.Bronchovesicular-moderate,
moderate pitch, over major bronchi
posterior between scapular
especially right anterior upper
sternum at 1st and 2ed intercostal
spaces
c.
c. Vesicular- Soft, low pitch, rustling sound of wind
through trees; over peripheral lung field
I. Decreased Sounds
• Obstruction- by secretion, mucus
plug or foreign body
• Loss of Elasticity- in lung fiber &
decreased force of inspired air
• Something obstructs transmission
of sound between lung and
stethoscope
2. No breath sounds- no air moving;
ominous sign
I.
I.
3. Increased breath sounds-
bronchial
sounds are abnormal when
heard
over abnormal location
i. Adventitious Sounds- sounds not
normally heard in the lungs; if
present are superimposed on breath
sounds
1. Crackles- rales
2. Wheeze – rhonchi
3. Atelectatic crackles-short,
popping, crackling sounds like fine
crackles
j. Voice Sounds-Vocal Resonance ; soft
muffled indistinct, heard through
stethoscope
1. Bronchophony-repeat “99”-
soft,muffled, indistinct heard through
stethescope cannot distinguish.
2.Egophony- auscultate chest
person phonates long “ee-ee-ee-
ee-” through stethoscope
3. Whispered pectoriloquy-
perslecton whispers phrase “one-
two-three”; response faint, muffled
and almost inaudible
• Normal Adult Respiration Patterns
– Rate- 10 to 20 breaths/minute
– Depth- 500 ml to 800 mo
– Pattern- even
– Ratio to Respiration- fairly constant 4:1
– Depth- air moving in & out each respiration
– Sigh- occasional normal pattern;
purposeful to expand alveoli
–
• Respiration Patterns:
• Tachypnea- rapid shallow breathing;
increased to >24
•
–
– Bradypnea- Slow breathing decrease but
regular; < 10/minute
– Cheyne-Stokes- breathing periods last 30
to 45 seconds, with periods of apnea (20
seconds); alternating the cycle
– Hyperventilation- Increase both in rate
and depth
– Hypoventilation- irregular shallow pattern
– Biot’s Respiration- similar to Cheyne-
Stokes except pattern is irregular
– Orthopnea- difficulty breathing when
supine
– Paroxysmal nocturnal dyspnea-is
awakening from sleep with SOB & needs
to be upright to achieve comfort
- Hyperventilation- rapid, deep breathing
causes carbon dioxide to be blown off
• Chest size changes-
– Inspiration- lung size increases;
diaphragm descends and flattens;
negative pressure air rushes in
– Expiration- chest size recoils;
diaphragm decreases in chest size
and relaxes; positive pressure air
flows out
•
• Abnormal Tactile Fremitus
– Increased tactile Fremitus-increased
density of lung tissue, thereby making a
better conducting medium for vibration
– Decreased Tactile Fremitus- anything
obstructs transmission of vibration.
– Rhonchal Fremitus- vibration felt when
inhaled air passes through thick
secretions in larger bronchi
– Pleural Friction Fremitus- inflammation of
the parietal or visceral pleura causes a
decrease
in normal lubricating fluid
• Adventitious Lung Sounds:
• Discontinuous Sounds- are discrete crackling
sounds
– Crackles-fine; formerly called rales, high-
pitched, short crackling, popping sounds
heard during inspiration cannot be
cleared by coughing
– Crackles-coarse; loud, low-pitched,
bubbling & gurgling sounds that start in
early inspiration and may be present in
expiration; sound like Velcro fastener
opening
– Atelectatic crackles; sound like fine
crackles, but do not last and are not
pathologic
– Pleural friction rub- is coarse & low pitch has,
Sounds is inspiratory and expiratory
• Continuous Sounds are musical sounds
– Wheeze- high pitched- musical sound that
sound polyphonic; predominately in
expiration but may occur in inspiration &
expiration
– Wheeze- low pitched- rhonchi; monophonic
single note; musical snoring; moaning
sound; more prominent on expiration; may
be cleared by coughing
– Stridor- high pitched- monophonic, crowing
sound, heard on inspiration
• Common Respiratory Conditions:
– Atelectasis-collapsed shrunken section
of alveoli or entire lung due to:
• Airway obstruction, Compression
on lung, Lack of surfactant
• Pt. exhibits-cough, increased pulse
& respiration, possible cyanosis
• None if bronchus obstructed;
occasional fine crackles is
bronchus patent
– Lobar Pneumonia- Consolidation;
• alveoli consolidated with fluid,
bacteria, RBC’s & WBC’s
• Crackles, fine to medium
•
– Bronchitis-proliferation of mucous glands in
passageway
• Bronchial inflammation and copious
secretions
• Deflated alveoli beyond obstruction
• Crackle over deflated area; may have
wheeze
• Pt. exhibits hacking rasping productive
cough
– Emphysema-destruction of pulmonary
connective tissue
• Over distended alveoli with destruction
of
• septa; permanent enlargement of
air sacs distal to terminal
bronchioles
• Pt. exhibits barrel chest, uses
accessory muscles to aid
respiration, SOB, tachy-pnea,
• Adventitious Sounds- usually
none; occasionally wheeze
– Asthma- allergic hypersensitivity to
certain inhaled allergens
• Bronchospasm
• Edema of bronchial mucosa
• Thick mucus
• Pt exhibit-SOB with audible
wheeze, retraction of intercostal
spaces, use of accessory
muscles,cyanosis
– Pleural Effusion- excess fluid in the
intrapleural space with compression of
overlying lung tissue
• Effusion maybe; Transudative
(watery capillary fluid),
Exudatative ( protein),
Empyemic (purulent matter)
Hemothorax (blood),Chylothorax
(Milky lymphatic fluid)
• Presence of fluid subdues lung
sounds
• No adventitious sounds
• Pt. exhibits-increased respirations,
dyspnea
dry cough, abdominal distention,
cyanosis
– Heart Failure- pump failure increasing
pressure of cardiac overload causes
pulmonary congestion
• Bronchial mucosa may be swollen
• Dependent airways deflated
• Adventitious Sounds-crackles at
lung base
• SOB, increased respiratory rate,
PND, nocturia, ankle edema
•
– Tuberculosis (TB) Tuberculosis-inhale
tubercle bacilli into alveolar wall
• Initial complex is acute
inflammatory
• Rust colored sputum
• Night sweats
• Low grade afternoon fever
• High incidence of Asian immigrant
•
– Initial complex is acute
inflammatory
• Scar tissue forms, lesion calcifies
• Reactivation of previously healed
lesion
• Extensive destruction as lesion
erodes into bronchus
• Adventitious sounds, crackles over
upper lobes, persist following full
expiration and cough
– Pneumocystis carinii Pneumonia
• Virulent form of pneumonia
associated with AIDS
• Cysts containing organism &
macro- phages form in
alveolar space; alveolar walls
thicken
• Adventitious sounds-crackles may
be present but often absent
•
– Pulmonary Embolism-undissolved
material originating in legs or pelvis,
detach
and travels and lodges to occlude
pulmonary vessels
• Sometimes occluded medium
pulmonary branches
• Client exhibits chest pain, worse on
inspiration, dyspnea, anxious,
apprehensive, Crackles and
wheezes
• Adventitious Sounds- Crackles,
Wheezes
– Acute Respiratory Distress Syndrome
(ARDS)
• Acute pulmonary insult, damages
alveolar capillary membrane,
increased permeability of pulmonary
capillaries, alveolar epithelium, to
pulmonary edema
• Adventitious Sounds- crackles, rhonchi
• Pt. exhibit-acute dyspnea,
apprehension, shallow rapid
breathing, thin frothy
sputum,retraction of intercostal
spaces
•
• Measurement of Pulmonary Function Status-
– Forced expiratory time-number of seconds it
– Pulse Oximeter- noninvasive method to
assess arterial oxygen saturation
(Spo2) Sensor attaches to client’s
finger detector measures amount of
light absorbed by oxyhemoglobin
(HbO2) and unoxygenated (reduced)
hemoglobin (Hb); ratio of light emitted
to light absorbed con converts to % of
oxygen saturation; Healthy person no
lung disease or anemia has a Spo2 of
97% to 98 %.
– 12 minute distance (12MD) walk, clinical
measure of functional status of clients
with COPD; used as outcome
measure for
people in pulmonary rehabilitation
• Infants and children
• Inspect and then listen to lung sounds of
infants sleeping, can concentrate on
breath sounds
• May sit in parents lap and play with
stethoscope reduces fear
• Older children like to listen to their own
lungs
A. Inspection
large
in relation to tiny chest.; note hypper-
resonance occurs normally in infants
and young child due to thin chest wall
E. Auscultation-normally bronchovesicular
breath sounds in infants up to 5-6 year
old; breath sounds are louder and
harsher
-fine crackles commonly heard
immediate
in newborns
-Cackles in upper lung field occur with
cystic fibrosis
-Expiratory wheezing occurs in lower
airway obstruction e.g., asthma,
bronchiolitis
-Stridor- high pitched inspiratory
crowing with upper arway
obstruction, e.g., croup, foreign body
aspiration, acute epiglottitis
– Depth of respirations-
• Hyperpnea- too deep
• Hypopnea- too shallow
– -Retraction- sinking in of soft tissue
relative to the cartilaginous and bony
thorax; in severe airway obstruction-
retraction extreme.
– Nasal flaring- sign of respiratory distress
– Head bobbing- in sleeping or exhausted
infant sign of dyspnea
– Noisy breathing- “snoring” obstruction,
polyps or foreign body in nasal
passages
– Grunting- sign of chest pain- acute
pneumonia/ pleural involvement
– Chest pain-older children maybe
pulmonary and or nonpulmonary
– Clubbing- proliferation of tissue about
the terminal phalanges, associated
with chronic hypoxia, chronic
pulmonary disease or primarily cardiac
defect
– Cough- maybe associated with
respiratory disease; is protective
mechanism
F. Tests-
– Pulse oximetry- similar to adults
however can position around foot, toe,
earlobe
– Transcutaneous Oxygen Monitor –Tc
Po2
measures O2 diffusion across skin
G. Oxygen Therapy
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The Cardiovascular System
•Functions:
•Delivery system for everything!
•Remove carbon dioxide and other
waste products
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The Heart
•Location
•Thoracic cavity, between the lungs
•In mediastinum
•Pointed apex directed toward left hip
•2/3 to left of median plane
•Size: About the same as your fist
•
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Location and Orientation within the Thorax
Figure 18.2
The Heart: Did You Know…
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The Heart: Coverings
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The Heart: Coverings
The Heart: Coverings
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Structure of the Heart –
Coverings
Figure 18.3
The Heart Wall
•Three layers
•Epicardium
•Outside layer
•This layer is the visceral pericardium
•Connective tissue layer
•Thin, shiny, slick
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Fig. 12.12
Structure of the
Heart Wall
Epicardium
= visceral
pericardium
Figure 18.3
The Heart: Heart Wall
•Myocardium
•Middle layer
•Mostly cardiac muscle
•Very thick
•Endocardium
•Inner layer
•Endothelium (Simple squamous E.T)
•Slick, shiny
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Structure of the Heart Wall
Fig. 12.12
Myocardium
Endocardium
Figure 18.3
The Heart: Chambers
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External Heart Anatomy
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The Heart: Chambers
•Ventricles
•Thick walled, lower chambers
•Pumping chambers
•Right ventricle:
•to pulmonary circuit (-O2
blood)
•Left ventricle
•To systemic circuit (+O2
blood)
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External Heart Anatomy
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The Heart: Valves
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Heart Valves and Major Blood Vessels
Superior Aorta
Vena cava
Pulmonary Arteries
Semilunar Pulmonary Veins
valve LA
RA
Bicuspid (mitral)
Tricuspid Valve
Valve LV
Inferior RV
Vena cava
Heart Valves
Figure 18.5c
The Heart: Valves
•
•Semilunar valves between ventricle and
artery
•“Passive”: depend on blood pressure
•Pulmonary semilunar valve
•RV to pulmonary trunk
•Aortic semilunar valve
•LV to aorta
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Heart Valves
Figure 18.5c
The Heart: Valves
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Heart Valves
Fig. 12.7
Figure 18.5c
Operation of Heart Valves
Fig. 12.9
Figure 11.4
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The Heart: Associated Great Vessels
•Great Arteries
•Aorta
•Leaves left ventricle
•Supplies systemic circuit
•Pulmonary trunk (artery)
•Leaves right ventricle
•Supplies pulmonary circuit
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Great Arteries
The Heart: Associated Great Vessels
•Great Veins
•Venae cavae (superior, inferior)
•Enter right atrium
•Drain systemic circuit
•Pulmonary veins (four)
•Enter left atrium
•Drain pulmonary circuit
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Great Vessels
Figure 18.5c
Coronary Circulation
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Coronary Circuit, Anterior View
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Coronary Circuit, Posterior View
The Heart: Conduction System
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The Heart: Conduction System
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The Heart: conduction system
Fig. 12.15
Figure 11.5
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The Heart: conduction
system
Fig. 12.15
Figure 11.5
•Impulse transmission
•AV Node serves as “booster station”
•Sends impulse through AV
bundle, along bundle branches
•Finally to Purkinje fibers
•Ventricle muscles contract
simultaneously
•
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Heart: conduction system
Figure 11.5
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Artificial Pacemakers
•implantable
•computer programmable
•sense heart rate and stimulate
as appropriate (e.g. during complete
heart block; next lecture)
lithium batteries
hybrid circuit
Pulse Generator
left atria
left ventricle
right atria
right ventricle
V V V V V V
normal ecg
A A A A A A
Artificial Pacemakers
•implantable
•computer programmable
•sense heart rate and stimulate
as appropriate (e.g. during complete
heart block; next lecture)
A A A A A A A A A
V V V V V
•Smooth Muscle
Local control of
blood flow
The Heart: Cardiac Cycle
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The Cardiac Cycle
Fig. 12.17
Figure 11.6
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Fig. 12.16
ECG
P wave:
Atrial depolarization.
QRS complex:
Ventricular
depolarization.
Atrial repolarization.
T wave:
Ventricular
repolarization.
electrocardiograph = a machine
that measures & records these
electrical signals
electrocardiogram = the reading produced
by this machine
the ECG is an important tool used to
diagnose abnormal heart rhythms &
patterns
heartbeat regulation
Heart Sounds
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Cardiac Output Regulation
Figure 11.7
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Overview of Stroke Volume Regulation
Blood Vessels
and
Circulation Slide 2.1
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The Heart: Regulation of Heart Rate
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Blood Vessels: The Vascular System
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The Vascular System
Figure 11.8b
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Blood Vessels: Anatomy
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Tunics of Elastic and Muscular Arteries
Fig. 13.1a
Figure 11.8b
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Blood Vessels: Anatomy
•Tunic externa
•Mostly fibrous connective tissue
•Provides support
•Prevents over-expansion of vessels
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The Vascular System
Figure 11.8b
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Differences Between Blood Vessel Types
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The Anatomy of Veins
Figure 11.8b
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Differences Between Blood Vessel Types
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Movement of Blood Through Vessels
•Arterial blood is
pumped by the heart
•Veins use the milking
action of muscles to
help move blood
Figure 11.9
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Vessels: Anatomy of a Capillary
•Capillaries
Fig. 13.3
•Form vast,
complex Slide 11.26
networks
•Walls one cell
layer thick
•Thin, leaky
•Allow for
exchange of
materials
•Capillary beds:
networks
•Vascular shunt: directly
connects an arteriole
to a venule
•
•
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Capillary Beds
•Exchange
vessels
•Oxygen and
nutrients
exit blood
•Carbon
dioxide and
waste
products
enter blood
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Blood Vessels: Did you know….
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Capillary Exchange
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Diffusion at Capillary Beds
Figure 11.20
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Special Circuits: Cerebral Arterial Circle
Fig. 13.10
Figure 11.13
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Special Circuits: Hepatic Portal System
Fig. 13.19
Figure 11.14
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Special Circuits: Fetal Circulation
Figure 11.15
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Pulse
•Pulse: pressure
wave of blood
•Caused by
contraction
of heart
•Monitored at
superficial
“pressure
points”
Figure 11.16
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Pulse
•Pulse – should
match heart
rate
•Averages 60-80
beats/minute
Figure 11.16
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Blood Pressure
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•
•Pressure in blood
vessels
•decreases
with distance
from the
heart
•Is lowest in
Slide 11.36
venous
system
Blood Pressure
Figure 11.18
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Factors Determining Blood Pressure
Figure 11.19
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Variations in Blood Pressure
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Variations in Blood Pressure
•
•Hypotension
•Low systolic (below 110 mm Hg)
•May be associated with illness
•Hypertension
•High systolic (above 140 mm Hg)
•High diastolic (above 90 mm Hg)
•Can be dangerous:
•stroke, heart attack, blindness
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Slide 2.1
BLOOD
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Blood
Figure 10.1
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Blood: Functions
•Transportation system
•Temperature regulation
•Acid-base balance (blood buffers)
•Protection
•Clotting
•Antibody production
•
•
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Physical Characteristics of Blood
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Physical Characteristics of Blood
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Blood Plasma
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Blood
Figure 10.1
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Plasma Proteins
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Formed Elements
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Erythrocytes (Red Blood Cells)
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make up 44% of the total volume of
blood
produced in the red bone marrow of the
ribs, humerus, femur, sternum, and
other long bones only have a nucleus in
the early stages of development
active about 120 days, then broken
down in the spleen & liver by
macrophages via phagocytosis
contain hemoglobin, an iron-rich protein
molecule that binds to O2
oxygenated RBC’s carry oxygen from
carbon dioxide in the blood:
Figure 17.3
Erythrocytes: Levels in Blood
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Fate of Erythrocytes
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Did you know…
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Erythrocytes: Disorders
•Anemias:
•Hemorrhagic: due to blood
loss
•Aplastic: RBCs not made
•Hemolytic: RBCs destroyed
•Polycythemia: too many RBCs
•
•
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Hemoglobin
•Iron-containing protein
•Binds reversibly to oxygen
•Each molecule has four oxygen binding
sites
•Each erythrocyte can carry 250 million
hemoglobin molecules
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Leukocytes (White Blood Cells)
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white blood cells (WBC’s): leukocytes
infection fighters
play a major role in protecting
you from foreign substances,
and from invading bacteria
make up 1% of total blood
volume
they are larger than RBC’s &
they have a nucleus
Types of Leukocytes
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Leukocyte Levels in the Blood
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Leukocyte Levels in the Blood
•Leukopenia
•Abnormally low leukocyte level
•<4000/mm3
•May be caused by certain drugs
•
•Leukemia: cancer of WBCs
•myeloid
•lymphoid
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Types of Leukocytes
•Granulocytes
•Granules in
their cytoplasm
can be stained
•Include
neutrophils,
eosinophils,
and basophils
Figure 10.4
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Granulocytes
•Multilobed nucleus
with
•Fine, pale purple
granules in cytoplasm
•Act as phagocytes
•Most numerous in
blood
•
•
•
•Neutrophils
Figure 10.4
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Granulocytes
•
Slide 10.11a
•Eosinophils:
•Large brick-red
cytoplasmic granules
•Respond to allergies
and parasites
•Rare in blood
•
•
•Eosinophils
Figure 10.4
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Granulocytes
•
•
•Basophils
Figure 10.4
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Agranulocytes
•Lymphocytes:
•Nucleus fills most of
Slide 10.12
the cell
•Major role in immunity
•“B” lymphocytes
•make antibodies
•plasma cells
•“T” lymphocytes:
mediate function of B
cells
Slide 10.10a
•Lymphocytes
Figure 10.4
Slide 10.12
•Monocytes:
•Largest of the white
blood cells
•Function as phagocytes
•Called
macrophages in
tissues
•Fight chronic infection
•
•
•Monocytes
Figure 10.4
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Platelets
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Types of Leukocytes
•
•
•Platelets
Figure 10.4
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Hematopoiesis
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Hematopoiesis
•
•
Figure 10.4
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•Stoppage of blood
flow
•Result of a break in a
blood vessel
•Hemostasis involves Slide 10.18
three phases
•Platelet plug
formation
•Vascular spasms
•Coagulation
Hemostasis: Blood
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Clotting
Platelet Plug Formation
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Hemostasis, con’t…
Slide 10.19
Fig. 11.8
•Platelet plug
formation
•
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Coagulation
•Injured tissues release thromboplastin
•Thromboplastin, clotting factors, and
calcium ions interact to trigger a clotting
“cascade”
•Prothrombin activator converts
prothrombin to thrombin (an enzyme)
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Coagulation
Fig. 11.9
Slide 10.21a
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Clot Retraction
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Blood Clotting
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Undesirable Clotting
•Thrombus
•A clot in an unbroken blood vessel
•Can be deadly
•Coronary thrombosis
•DVT: deep vein thrombosis
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Thrombus in Artery
Undesirable Clotting
•Embolus
•Clot moving through a vessel
•Can be deadly in areas like the brain,
lung
•Pulmonary embolism
•Cerebral embolism
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Bleeding Disorders
•Thrombocytopenia
•Platelet deficiency
•Causes bleeding from small blood vessels
•Can result from chemo, radiation
•May be age-related
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Bleeding Disorders
•
•Hemophilia
•Hereditary bleeding disorder
•Normal clotting factors are missing
•Many types, depending on clotting factor
•A gene mutation: Queen Victoria
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Blood Groups and Transfusions
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Blood Groups and Transfusions
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Human Blood Groups
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Human Blood Groups
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Blood Typing
Blood antigens
Type A
Type B
Agglutininins (Ab)
Act in blood typing
Antigen-antibody reaction
Human Blood Groups
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ABO Blood Groups
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Blood Types and their
corresponding Abs
Type A, anti-B
Type B, Anti-A
Type AB, neither
Blood Groups
Type O, both
Rh Blood Groups
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Rh factor = Rhesus factor:
another antigen which may be
present (Rh+) or absent (Rh-)
Rh factor is an inherited
characteristic
only 15% of the U.S. population is
Rh-
Rh Dangers During
Pregnancy
•Called hemolytic disease of
the newborn or
Erythroblostosis fetalis
•Danger is only when
•the mother is Rh–
•the father is Rh+
•the child inherits the
Rh+ factor
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Rh Dangers During Pregnancy
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prevention: mom is treated with a
substance to prevent the production of
antibodies in her blood at 28 weeks & again
shortly after the birth of the first baby
Rh Dangers During Pregnancy
•Erythroblostos
is fetalis, or
•Hemolytic
Slide 10.29b
Fig. 11.13
disease of the
newborn
•
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Blood Typing
Blood Typing
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Lymphatic
System and
Immunity
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The Lymphatic System
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Lymphatic Characteristics
•Lymph
•Tissue fluid in lymphatic vessels
•Body produces ~3L/day (how much
blood do we have???)
•Properties of lymphatic vessels
•One way system toward the heart
•No pump
•Assisted by skeletal muscle
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Lymphatic Vessels
•Lymph Capillaries
•“Blind tubes”
•Walls have valves
•Fluid leaks into lymph capillaries
•Higher pressure inside closes valves
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Lymphatic Vessels
Figure 12.1
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Lymphatic Vessels
•Lymphatic vessels
•Collect lymph
from lymph
capillaries
•Carry lymph to
nodes
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Lymphatic Vessels
•Lymphatic vessels
(continued)
•Returns fluid to
subclavian veins
•Right
lymphatic
duct
•Thoracic
duct
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Lymph
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Lymph
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Lymph Nodes
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Lymph Nodes
Figure 12.3
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Lymph Node Structure
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Lymph Node Structure
Figure 12.4
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Other Lymphoid Organs
•
•Spleen
•Thymus
•Tonsils
•Peyer’s
patches
Figure 12.5
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The Spleen
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The Thymus
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Lymphoid Organs
Thymus:
atrophies
with age
Spleen: can
live without
this
Figure 20.8
Tonsils
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Peyer’s Patches
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Fig. 14.3
Lymphoid Organs
Tonsils: 3
sets
Peyer’spatche
s: part of
GALT
Figure 20.8
Body Defenses
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Body Defenses, con’t…
Slide 12.15b
•Specific or
F ig. 14.15
Acquired
defense system:
Cell Mediated
response
•Specific
defense is
required for
each type of Cell mediated
invader response
•T-cells:
viruses, fungi,
cancer cells
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Acquired Defenses, con’t…
Fig. 14.11
Slide 12.15b
•Humoral
Immunity
•T-cells
influence B-
cells
•B-cells:
Bacteria
•B-cells make
antibodies
(Ab) Humoral Immunity: Ab
•Ab circulate in production
blood
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Nonspecific Body Defenses
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Defensive Cells
•Phagocytes
•Neutrophils
•Monocyte/
Macrophages
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Defensive Cells
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Inflammatory Response is the
Second Line of Defense: FYI
•Triggered by injury
•Produces four signs
•Redness
•Heat
•Swelling
•Pain
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Functions of the Inflammatory Response:
FYI
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Steps in the Inflammatory Response: FYI
Figure 12.7
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Antimicrobial Chemicals: FYI
•Complement
•Protein cascade
•Kills invaders
•Interferon
•Proteins secreted by virus-infected cells
•Inhibit virus binding to healthy cells
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Fever: FYI
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Lymphatic
System and
Immunity
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Specific Defense: The Immune Response
•Characteristics:
•Antigen specific: for a particular
foreign substance
•Systemic: affects entire body
•Has memory: protects against
future infection
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Types of Immunity
•Humoral immunity
•Targets bacteria
•B-lymphocytes
•Cell-mediated immunity
•Targets virus infected cells, cancer
•T-lymphocytes
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Antigens (Non-self)
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Cells of the Immune Response
•Lymphocytes
•B lymphocytes mature in the bone marrow
•Make plasma cells that make
antibodies
•T lymphocytes mature in the thymus
•Memory Cells: from B or T cells
•Macrophages
•Arise from monocytes
•Most live in lymphoid organs
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Cells of the Immune Response
Slide 12.29
Fig. 14.17b
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Activation of Lymphocytes; FYI
Figure 12.9
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Vaccinations and Booster Shots: FYI
Figure 12.11
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Antibody Structure: for Lab…
•Four peptides
linked by
covalent bonds
•Two heavy
chains
•Two light chains
•Recombinant
DNA!
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Organ Transplants and Rejection: FYI
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Organ Transplants and Rejection: FYI
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Disorders of Immunity:
Immunodeficiencies (FYI)
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Autoimmune Diseases (FYI)
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Autoimmune Diseases: FYI
•Examples:
•Multiple sclerosis
•Myasthenia gravis
•Type I diabetes
•Rheumatoid arthritis
•Systemic lupus erythematosus (SLE)
•Glomerulonephritis
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 12.50b
Neurological ANATOMY &
PHYSIOLOGY
WITH
Health Assessment
Four Types:
Astroglia,
oligodendroglia,
ependyma &
microglia
The Neuron: Cellular Impulses
Action Potentials
body functions.
Composed of both gray matter and white matter.
Protective Mechanisms:
Skull (cranium): Bony container surrounding the brain
Meninges: Three additional layers of protection
Dura mater, arachnoid mater & pia mater
Potential & Actual Spaces
Epidural Space
Subdural Space
Subarachnoid Space
Cerebrum
Divided into two hemispheres:
Right Hemisphere
The right side of the brain controls & receives
information from the left side of the
body.
Left Hemisphere
The left side of the brain controls & receives
information from the right side of the body.
Dominant hemisphere in most people
Lobes of the Cerebrum
Frontal Lobe
Midbrain:
Aqueduct of Sylvius
Pons:
Cardiac & Respiratory Centers (rate & length)
Medulla Oblongata:
Auditory, Cardiac & Respiratory Center (basic
rhythm)
Cerebral Circulation
Arterial Circulation:
Circle of Willis
Internal carotid, basilar artery & the anterior,
middle & posterior arteries join together via
small communicating arteries to form a ring
at the base of the brain.
Venous Circulation:
Vertebral Column
Intervertebral Disks
Meninges
Peripheral Nervous System (PNS)
Spinal Nerves (31 pairs)
Mixed Nerve Fibers: Exiting the spinal cord to
receive information and to transmit
information to the cord → brain.
Posterior Root = Sensory
Anterior Root = Motor
Reflex Arc
Interneurons connecting sensory & motor fibers.
Dermatomes
Sensory depiction of the corresponding spinal
nerves
*See Smeltzer & Bare pp. 1829; Figure 6
PNS: Cranial Nerves
There are 12 pair of cranial nerves.
CN V Trigeminal:3
branches;
sensation to the face,
cornea and scalp;
opens jaw against
resistance
CN VII
Facial: moves the
face; taste
Neuro
Assessment
Cranial Nerves
CN VIII
Acoustic: 2
branches, acoustic (hearing)
and
vestibular (balance)
CN IX
Glossopharyngeal:
moves the
pharynx (swallow,
speech & gag)
CN X
Vagus:
voice quality
Neuro Assessment
Neuro Assessment
Cranial Nerves
* Test enough times to ascertain validity of
responses
Sensory Assessment
Light Touch
• Client sitting
• Eyes closed
• “Say where you are
touched.”
• Compare bilaterally,
and distally to
proximally.
•
Vibratory Sensation
• Close eyes
• Strike fork & start on
most distal bony
prominence & work
medially with
neuropathy
• Ask when do you feel
the vibration start
and when do you
feel the vibration
stop.
Stereognosis
• Close eyes
• Place object in hand
• “Identify object.”
• Test bilaterally with
different objects.
• Note speed and
accuracy
• Astereognosis –
unable to identify
object
Graphesthesia (Parietal Lobe)
• Close eyes
• Draw letter or
number on hand
• “Identify figure.”
• Test bilaterally
• Note speed and
accuracy
• Agraphesthesia –
inability to identify
figure
Reflexes
Reflex Charting
• 4+ - Hyperactive,
commonly with
clonus
• Clonus – continued
movement after
stimulations removed
DTR Testing
Abnormal Reflexes
Biceps Reflex
• Support the client’s
forearm
• Client’s arm flexed at
45-90 degree angle
• Hold arm loosely
• Strike tendon with a
brisk wrist motion
on top of your
thumb
Brachioradialis Reflex
Triceps Reflex
• Relaxed arm
required.
• extension of the
forearm.
Patellar Reflex
• Sit on edge of table
with leg hanging
free.
• Place hand over
quadriceps muscle
• Strike patellar tendon
just below the
patella – blunt end of
hammer
Achilles Reflex
• Loosely support foot
in hand.
• Briskly strike Achilles
tendon.
• Plantar flexion of the
foot.
Abdominal Reflex
Plantar Reflex
• Stroke up the lateral
side of the sole &
across the ball of
the foot to just
below the great toe.
• Plantar flexion of the
toes, normal
response.
• Negative Babinski
sign.
Meningeal Irritation
Neurosurgery Considerations
Newborn Considerations
Newborn Reflexes
Plantar
Moro Reflex
Tonic Neck
Babinski
• Positive Babinski
reflex – normal with
infant
• Abduction of the toes
with dorsiflexion of
the great toe
Placing & Stepping Reflex
Gerontological Variations
Normal Findings after 65
Brain Teaser
QUESTIONS
Question 1
Question 2
Question 3
Neurological Disorders
DENNIS N. MUÑOZ, R.N., R.M.
Neurological Assessment
Health History
General Signs & Symptoms
Level of Consciousness
Motor Function
Pupillary Function / Eye Movements
Vital Signs
Respiratory Patterns
Laboratory & Diagnostic Testing
Neurological Health History
Explore Presenting Compliant (s) → “OLD
CART”
Precipitating Events
Traumatic Event Data
too).
Progression of signs / symptoms
Client Information
Allergies
Past Medical & Surgical History
Medications
Habits / Lifestyle Changes
Familial History of Neurologic Disorders
General Signs / Symptoms
Three Categories:
Eye opening
Best motor response
Best verbal response
Scoring
Highest or best possible score 15
A score of < 8 indicates coma
Lowest or worst possible score 3
Not appropriate for use in:
Children, intoxicated clients or spinal cord injuries
Motor Assessment Techniques
Steps of Examination:
Observe for spontaneous movement
Elicit motor movement in response to stimuli
Types of Stimuli:
Verbal
Simple and direct statements; no visual or tactile
stimuli
Reduce environmental stimuli or distractions
Noxious (painful)
When no response to verbal stimuli
Acceptable methods: nail bed pressure, trapezius
pinch & supraorbital pressure (not used with
head injury).
Motor Responses
Abnormal Motor Responses
Flaccidity
↑ Decorticate
↑ Decerebrate
Motor Assessment Cont.,
Motor Movements & Strength
Size (mm)
Shape
Reactivity to Light
Extraocular Movements (EOM)
CN III, CN IV and CN VI
Ocular Responses Cont.,
Ocular Reflexes (unconscious client)
Cheyne-Stokes
X-rays
MRI
CT Scans
Position Emissions Tomography (PET) Scans
A radioactive substance is either inhaled or
injected to provide images of the brain’s
function.
Used to assess blood flow, tissue composition &
brain metabolism, therefore it indirectly
measures brain function.
Diagnostic Testing
Cerebral Angiography
Normal Findings:
pH 7.35-7.45
Specific Gravity: 1.007
Appearance: Clear, colorless and odorless
Cells: minimal number of WBCs and no RBCs
Positive Protein
Positive Glucose (2/3 blood sugar value)
Intracranial Pressures (ICP)
Brain contained within the skull (closed
container)
Intracranial space is occupied by three
components:
Blood (10%)
Cerebral Spinal Fluid (CSF) (10%)
Brain Tissue (80%)
Normal physiologic conditions ICP < 10 mmHg
An ICP value of 20 mmHg (sustained) requires
Intracranial Pressures (ICP)
Cont.,
Monro-Kellie Hypothesis:
neurologic damage.
Clinically - CPP is maintained by either increasing
MAP or decreasing ICP.
Clinical Manifestations:
Stages of Increased ICP
Stage I: (Full Compensatory)
Comatose
Pupillary dilation & fixation (ipsilateral →
bilateral)
Abnormal Posturing:
Decorticate → Decerebrate → Flaccidity
Cushing’s Triad Progresses To:
Narrowing pulse pressure
Weak, thready pulse
Respirations: Cheyne-Stokes → Ataxic
Respirations
Stage V (Death)
ICP Monitoring
Intraventricular
A small catheter is placed within the ventricular
system (ventriculostomy); allows for CSF
drainage.
Subarachnoid
Hollow bolt or screw into the subarachnoid space
Epidural
Small fiberoptic sensor into epidural space
(between skull & dura)
Intraparechymal
Small fiberoptic catheter into the white matter of
brain tissue (parenchyma)
Increased ICP: Medical Management
Sedatives
Benzodiazepines i.e. lorazepam (Ativan)
Neuromuscular Blockade / Paralyzing Agents
i.e. vecuronium (Norcuron)
Must still provide sedation and / or pain management !!
Barbiturate Therapy (Induced Coma)
i.e. pentobarbital or thiopental; used when conventional
medical interventions fail to reduce ICP; controversial.
Increased ICP: Medical Management
Other Medical Interventions:
Temperature Regulation
Prevent Hyperthermia (i.e. antipyretics, ice packs &
cooling blankets)
Blood Pressure Regulation
Delicate balance in the client with increased ICP; often
maintained on the high end of normal to ensure
adequate cerebral perfusion!!
Sedatives often enough, if not antihypertensive agents
used
Seizure Control / Prevention
Antiseizure Agents i.e. phenytoin (Dilantin)
Increased ICP: Nursing
Considerations
Nursing Assessment / Monitoring
Frequent Vital Signs & Neurological Exams
Trends in signs and symptoms are paramount !!
Report deterioration of neurologic status promptly
Maintain ICP monitoring device
Document amount & appearance of CSF drainage
Aseptic technique with dressing changes
Strict I & O and Daily Weights
Laboratory Values
i.e. CBC, SMA 7, Electrolytes & ABG’s
Increased ICP: Nursing
Considerations
Nursing Activities
Transsphenoidal
Craniotomy Considerations
Preoperative Nursing Care
Assessment
Frequent vital signs and neurological exams
Documentation of neurological baseline
Diagnostic / Laboratory Tests
Blood tests / blood type and cross match
Chest x-ray and 12 lead EKG
Education
Avoid activities known to increase ICP
Surgery specific instructions
Provide Emotional Support
Craniotomy Considerations
Postoperative Nursing Management
Prevent Injury
Seizure / Falls Precautions
Eye Care / Skin Care
Providing Emotional Support
Patient Education
Signs & symptoms of increased ICP
Signs & symptoms of infection
Incisional care
Medications
Neurologic Rehabilitation
Stress importance; PT / OT consults helpful .
Craniotomy Considerations
Complications
Increased ICP
Surgical Hemorrhage
Fluid / Electrolyte Imbalance
CSF Leak
DVT
Gastric Ulcers
Pneumonia
Seizures
Complications of Increased ICP
• Diabetes Insipidus
• SIADH (Syndrome of Inappropriate Antidiuretic
Hormone)
• Herniation
• Brain Death
Diabetes Insipidus
Decreased secretion of antidiuretic hormone
(ADH)
Clinical Manifestations:
Hypernatremia (serum)
Excessive water losses via urine (↑ UO)
Client may experience volume depletion !!
Management:
Fluid Volume Replacements
Encourage oral intake of fluids (if possible)
I.V. fluids; careful monitoring: laboratory results and
BP
Electrolyte Replacements
Vasopressin therapy:
Pitressin or Desmopression DDAVP
SIADH
Increased secretion of antidiuretic hormone
(ADH)
Clinical Manifestations:
Hyponatremia (serum)
Decreased water losses via urine (↓ UO)
Volume overload (i.e. weight gain)
Management:
Deformation Injuries
Occurs when an object strikes the head
Often resulting in skull fractures, concussion,
contusion or intracranial hemorrhage.
Causes: baseball bat or bottle
TBI: Mechanisms of Injury
Cont.,
Blunt, Non-Missile Injuries
Acceleration-Deceleration Injuries
Also, called Coup-Contrecoup Injuries
When the brain rapidly accelerates
and decelerates within the skull.
Two areas of brain injury:
Site of impact
Opposite side of the brain
Often resulting in contusions & intracranial
hemorrhage
Cause: Motor vehicle collision (MVC)
Scalp Injuries
• Isolated scalp injuries usually classified as
minor head injuries.
• The scalp is highly vascular with poor
constrictive abilities; bleeding is often
profuse
• Infection is a major concern, which must be
prevented!!
Skull Fractures
Actual break in continuity of skull
Linear:
Non-displaced fracture of the skull
Depressed:
Fracture involving the downward depression of bone into
brain tissue
Comminuted:
Fragmentation and downward displacement of bone into brain
tissue
Basilar:
Skull Fractures Cont.,
Basilar Skull Fractures
Epidural hematoma
Subdural hematoma
Intracerebral hematoma
Epidural Hematoma (EDH)
Blood collects between the dura mater & the
skull
Most often arise from arterial hemorrhage
Cause usually is injury of middle meningeal artery;
resulting in rapid accumulation of blood.
Clinical Manifestations:
+ LOC after initial trauma; usually at the location of
injury
Lucid interval (30-50% experience)
Rapid deterioration in neurologic status; S/Sx of ↑ ICP
Management
Medical emergency requiring immediate medical and
Subdural Hematoma (SDH)
Blood collects between the dura mater & the
arachnoid mater
Often originating from venous hemorrhage
Cause is usually injury to bridging veins; venous blood
tends to accumulate more slowly than arterial blood,
therefore signs/symptoms of ↑ ICP tend not occur as
quickly.
Two Main Types of SDH
Acute (less than 48 hours after injury)
Requires immediate medical and /or surgical intervention
Chronic (over 2 weeks after injury)
Often forget actual injury; common in elderly
S/Sx of ↑ ICP fluctuate or “come and go”
Management: Burr hole clot evacuation or craniotomy
Intracerebral Hematoma (ICH)
Blood collects within the brain tissue
(parenchyma)
Bleeding causes displacement of brain tissue; even
small bleeds can cause significant neurological
alterations.
Destroys brain tissue
Causes cerebral edema
Increases ICP
S/Sx of ↑ ICP maybe be immediate or develop
overtime
Management:
Depends on location of the bleed and size of the
bleed
TBI: Management
Considerations
Medical / Surgical Management
Supportive Interventions
Prevention or Management of Increased ICP
Airway
Ventilation
Nutrition
Pain and anxiety management
Prevention of seizures & agitation
See previous discussion of medical / surgical
management of increased ICP
TBI: Management
Considerations
Nursing Considerations
Benign or malignant.
Clinical manifestations differ according to area of
lesion and rate of growth
Common Signs / Symptoms:
Alterations in consciousness
Neurologic deficits
Motor & Visual Disturbances
Headaches
Seizures
Vomiting (maybe sudden and projectile)
Types of Brain Tumors
Brain tumors within the brain tissue
Meningiomas
Encapsulated, non-invasive; usually benign
Slow growing; well defined
Compresses rather than invades
Acoustic Neuromas
Non- malignant ; slow growing
CN VIII affected: HA, tinnitus, hearing loss, impaired
balance, unsteady gait & facial pain / numbness on the
side of tumor
Developmental Tumors
Angiomas
A benign mass of abnormal blood vessels with thin
walls; prone to rupture
Brain Tumor: Management
Considerations
Increased Intracranial Pressure
Pharmacologic Agents
Corticosteroids (dexamethasone and prednisone)
H2 blocker or proton pump inhibiter must accompany
Osmotic Diuretics
Antiseizure, antiemetic & analgesic medications
See previous discussion of ↑ ICP management
& nursing considerations
Tumor Removal / Destruction
Surgical Interventions
Craniotomy
ICP monitoring
Brain Tumor: Management
Considerations
Tumor Removal / Destruction Cont.,
Medical Interventions
Chemotherapy (often a combination of agents
utilized)
Routes of Administration
Intrathecal Route
Intracranial Route
Disk-shaped drug wafers (Gliadel wafers) maybe
implanted for some tumors (i.e. glioblastomas
multiforme or recurrent tumors) during a craniotomy.
Systemic / Venous Route
Most agents poorly penetrate the blood-brain barrier
Temodar (temozolomide) can penetrate; widely used
Brain Tumor: Management
Considerations
Radiation Therapy
Digestive System
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 2.1
The Digestive System
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 14.1
FUNCTIONS OF THE DIGESTIVE
SYSTEM
muscular contractions)
3. mechanical digestion = physically
form of feces
Extrinsic innervation:
Figure 14.1
Slide
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14.2b
Organs of the Digestive System
•Two components
•Alimentary canal – continuous coiled
hollow tube
•Accessory digestive organs –
everything else
Slide
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14.2a
Organs of the Alimentary Canal
•Mouth
•Pharynx
•Esophagus
•Stomach
•Small intestine
•Large intestine
•Anus
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Organs of the Digestive System
Figure 14.1
Slide
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14.2b
Mouth (Oral Cavity) Anatomy
•Lips (labia)
•Cheeks
•Hard palate
•Soft palate
•Uvula
Figure 14.2a
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MOUTH oral cavity
• mechanical digestion =
biting & chewing food
(mastication)
• chemical digestion =
breaking starches
(polysaccharides) into
disaccharides using the
enzyme amylase
MOUTH oral cavity
different teeth do
different jobs: 32
total
incisors cut /
bite
canines or
cuspids tear
& shred
premolars &
molars
MOUTH
Functions of saliva:
Figure 14.2a
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Mouth (Oral Cavity) Anatomy
•Tonsils
•Palatine
tonsils
•Lingual tonsil
Figure 14.2a
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Digestive Functions of the Mouth
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Digestive Functions of the Mouth
•Mechanical digestion
•Food broken down by chewing
•Chemical digestion
•Food mixed with saliva
•Starch digestion begins
Slide
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14.48
Pharynx Anatomy
•Nasopharynx
•Oropharynx: posterior
to oral cavity
•Laryngopharynx:
•posterior to
larynx
•Connects to
esophagus
Figure 14.2a
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ESOPHAGUS gullet
• runs from the pharynx through the
diaphragm to the stomach
• about 10 inches long, conducts peristalsis
to move food along
• heartburn or acid reflux disease result
when gastric juices backflow into the
esophagus
Pharynx Function
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Esophagus
Slide
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14.10
Activities of the Pharynx and
Esophagus
Slide
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14.49
Deglutition (Swallowing)
Figure 14.13
Slide
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14.52
Swallowing
• A programmed all-or-none reflex
• Chewing and moving the bolus of food back is manly
voluntary (striated muscle)
• Pressure of bolus on pharynx triggers involuntary reflex
(smooth muscle)
• Tongue prevents food from moving back
• Uvula elevated, sealing nasal passage
• Larynx elevates and closure of glottis
• Respiration briefly inhibited
• Pharyngeal muscles force bolus back
• Peristaltic waves move bolus through esophagus
•
PERISTALSIS
Ringlike
contraction
sweeps down
the esophagus
Layers of Organs in Alimentary
Canal
•Mucosa
•Innermost layer
•Simple columnar E.T.
•Lots of Goblet cells
•Protects, secretes, absorbs
Slide
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14.11a
Layers of Alimentary Canal Organs
Figure 14.3
Slide
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14.13
Layers of Alimentary Canal Organs
•Submucosa
•Deep to mucosa
•Loose connective tissue
•blood vessels
•nerve endings
•lymphatics
Slide
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14.11b
Layers of Alimentary Canal Organs
Figure 14.3
Slide
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14.13
Layers of Alimentary Canal Organs
Slide
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14.12
Layers of Alimentary Canal Organs
Figure 14.3
Slide
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14.13
Review!!!!!!!!!
Mucosa
Secrete mucus.
Submucosa
lymphatic vessels.
Submucosal plexus (Meissner’s plexus):
layers.
Major nerve supply to GI tract.
peptides
hydrochloric acid (HCl) lowers the pH to 2
Slide
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14.15a
Stomach Anatomy
Figure 14.4a
Slide
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14.17
Stomach Anatomy
Slide
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14.15b
Stomach Anatomy
Slide
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14.16a
Stomach Anatomy
Slide
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14.16b
Stomach Anatomy
Figure 14.4a
Slide
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14.17
Stomach Functions
Slide
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14.18
Specialized Mucosa of the
Stomach
•Simple columnar epithelium
•Gastric glands – secrete gastric juice
•Chief cells – produce pepsinogens
•Parietal cells – produce hydrochloric acid
•Endocrine cells – produce gastrin
Slide
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14.19
Structure of the Stomach Mucosa
•Gastric pits
•formed by folded mucosa
•Glands and specialized cells
•are deeper in the gastric gland region
Slide
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14.20a
Structure of the Stomach Mucosa
Figure 14.4b, c
Slide
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14.20b
FACTORS INFLUENCING
GASTRIC MOTILITY
• Distension of stomach: increases
• Feedback from the small intestine:
decreases
• Control from CNS
• Gastrin: increases
FACTORS CONTROLLING
STOMAC EMPTYING
• Gastric Motility
• Enterogastric reflex: Via intrinsic and
autonomic nerves
• Enterogastrones: secretin, cholecystokinin
(CCK), gastric inhibitory peptide
•
FACTORS IN SMALL INTESTINE CONTROLLING
STOMAC EMPTYING
• Fat
• Acid
• Hypertonicity
• Distension
Small
Intestine
the Small
Intestine
•Duodenum
•Attached to the stomach
•Curves around the head of the pancreas
•Jejunum
•Second portion, ~8’
•Ileum
•Longest portion, ~10’
Slide
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14.23a
Chemical Digestion in the Small
Intestine
Figure 14.6
Slide
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14.23b
Villi of the Small Intestine
•Fingerlike
structures formed
by the mucosa
•Provide more
surface area
Figure 14.7a
Slide
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14.24
Structures Involved in Absorption
of Nutrients
•Absorptive cells
•Blood capillaries
•Lacteals (specialized
lymphatic capillaries)
Figure 14.7b
Slide
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14.26
Folds of the Small Intestine
Slide
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14.27
SMALL INTESTINE
uses pancreatic amylase to turn
starch into disaccharides
uses trypsin to turn proteins into
peptides
uses pancreatic lipase to turn fats
into fatty acids & glycerol
uses nucleases to turn nucleic
acids into nucleotides
SMALL INTESTINE
monosaccharide
sucrase turns sucrose into a
monosaccharide
lactase turns lactose into a monosaccharide
SMALL INTESTINE
Slide
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14.28
Large Intestine
Figure 14.8
Slide
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14.28
LARGE INTESTINE “colon”
• anaerobic bacteria synthesize vitamins B
and K
• major divisions: cecum, appendix, colon,
rectum, anal canal
• the appendix hangs from the 1st section
on the right side and may
become inflamed = appendicitis
LARGE INTESTINE “colon”
• the colon’s main regions are the
ascending colon, the transverse colon,
the descending colon, and the sigmoid
colon
LARGE INTESTINE “colon”
•Absorption of water
•Eliminates indigestible food as feces
•Does not participate in digestion
•Goblet cells produce mucus for
lubrication
Slide
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14.29
Functions of the Large Intestine
Slide
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14.29
Structures of the Large Intestine
Slide
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14.30a
Structures of the Large Intestine
•Colon
•Ascending
•Transverse
•Descending
•Sigmoid (S-shaped)
•Rectum
•Anus – external body opening
Slide
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14.30b
Large Intestine
Figure 14.8
Slide
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14.28
Modifications to the Longitudinal
Layer of Muscle
Slide
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14.31
Accessory Digestive Organs
•Salivary glands
•Teeth
•Pancreas
•Liver
•Gall bladder
Slide
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14.32
Organs of the Digestive System
Figure 14.1
Slide
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14.2b
Salivary Glands
Slide
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14.33
Saliva
•Mixture of mucus and serous fluids
•Helps to form food into a bolus
•Contains salivary amylase
•starch digestion
•Dissolves chemicals for taste buds
•We produce ~1 liter/day
Slide
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14.34
Teeth
Slide
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14.35a
Teeth
•Permanent teeth
•Replace deciduous teeth beginning ~6
years of age
•A full adult set is 32 teeth
•some people do not have wisdom
teeth
Slide
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14.35b
Classificatio
n of Teeth
•Incisors (2)
•Canines (1)
•Premolars (2)
•Molars (3)
•Same number and type of teeth in each
“quadrant” so….
•“Dental Formula”: 2-1-2-3
total
uincisorscut / bite
ucanines or cuspids tear &
shred
upremolars & molars crush /
grind
Classification of Teeth
Figure 14.9
Slide
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14.36b
liver: weighs 3 pounds
produces bile to emulsify fats
(mechanical digestion)
bile travels from the liver to the
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14.39
Primary Function of Liver
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14.40
Role of the Liver in Metabolism
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14.77
Gall Bladder
ugall
bladder:
«stores bile
produced by the
liver
«may be surgically
removed, but that
decreases a
person’s ability to
digest fats
efficiently
•Sac attached to inferior surface of liver
•Stores, concentrates bile
•Bile enters duodenum in the presence of fatty food
•Requires hormonal signals, autonomic innervation
•Gallstones can cause blockages
gland
secretes digestive
enzymes and
hormones
Pancreatic juice (pH
8) is bicarbonate
rich & it neutralizes
the acidic chyme as
it leaves the
stomach
Pancreas
•Exocrine function: Produces digestive enzymes
•Enzymes: secreted into duodenum
•Bicarbonate ions: neutralize acidic chyme
•Endocrine products of pancreas
•Insulin
•Glucagon
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14.38
Processes of the Digestive System
Figure 14.11
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14.46
Control of Digestive Activity
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14.47a
Control of Digestive Activity
•Stimuli include:
•Stretch of the organ
•pH of the contents
•Presence of breakdown products
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14.47b
Control of Digestive Activity
•
•Reflexes include:
•Activation or inhibition of glandular
secretions
•Smooth muscle activity
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14.47b
Digestion and Absorption in the
Stomach
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14.55
Digestion in the Small Intestine
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14.57a
Digestion in the Small Intestine
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14.57b
Stimulation of the Release of
Pancreatic Juice
•Vagus nerve
•Local hormones
•Secretin
•Cholecystokini
n
Figure 14.15
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14.58
Absorption in the Small Intestine
•Water
•Products of digestion
•Most molecules absorbed by active
transport
•Lipids absorbed by diffusion
•Nutrients transported to the liver
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14.59
Nutrition
•Nutrient – substance used by the body
for growth, maintenance, and repair
•Categories of nutrients
•Carbohydrates
•Lipids
•Proteins
•Vitamins
•Mineral
•Water
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14.63
Cellular Metabolism
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Cellular Metabolism, con’t…
•Carbohydrates
•Monosaccharides = simple sugars
•Glucose, fructose
•Disaccharides = Combinations of
monosaccharides, removal of water
•Sucrose, lactose, maltose
•Polysaccharides: usually
polymers of glucose
•Starch, cellulose, chitin
•
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14.67
Cellular Metabolism, con’t…
•Lipids
•1 glycerol + 3 fatty acids
neutral fat + 3 H2O
•These are triglycerides
•Further modifications
produce:
•Phospholipids (cell
membrane)
•glycolipids (cell
membrane)
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•Lipoproteins (cell 14.67
Cellular Metabolism, con’t…
•Proteins
•Two amino acids a dipeptide
+ H2O
•Covalent bond formed is a
peptide bond
•Unique to proteins
•Polypeptides: 2-100 amino
acids
•Protein: >100 amino acids
•Require additional
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modification to become 14.67
Cellular Metabolism, con’t…
•Proteins
•Modification occurs on four levels
•Primary: string of amino
acids
•Secondary: helix or “pleat”
structures
•Tertiary: 3-D folding
•Quarternary: two or more 3-
D proteins that act as a
functional unit
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14.67
Cellular Metabolism, con’t…
•Proteins
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14.67
Cellular Metabolism, con’t…
•Proteins
•May be structural or functional
•Structural:
•Play a role in cellular
architecture
•Collagen, fibrin, actin,
myosin, etc.
•Functional:
•Play a role in cell
metabolism
Slide
•Enzymes, neurotransmitters,
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14.67
Cellular Metabolism, con’t…
•Enzymes:
•Biological catalysts
•Highly specific for a substrate
•Substrate: substance upon
which an enzyme acts
•i.e., peptidases act
only on peptide bonds
in small polypeptides
•Produced only in presence of
substrate
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14.67
Cellular Metabolism, con’t…
•Enzymes:
•Huge protein molecules
•Alter shape to conform to
shape of substrate (“wrap
around” effect)
•Average 1500/cell (>5000 in liver
cells)
•Most require co-enzymes
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14.67
Cellular Metabolism, con’t…
•Enzymes:
•Recognize substrate by
shape of binding site
•Serve to lower energy
required for reaction to occur
(activation energy)
•therefore speed up reactions
•Not changed or used up during
reaction
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14.67
Cellular Metabolism, con’t…
•Co-Enzymes:
•Required to activate enzymes
•Facilitate enzymatic reactions
•May be a metal ion (Zn++ , Cu++ ,
Fe++ )
•May be a vitamin
•Vitamins are co-enzymes
•Only function if “their”
enzyme is available
• Slide
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14.67
Cellular Metabolism
• Catabolism: substances are broken
down into molecules
• “destructive” process
• Large molecules broken down into
smaller molecules
• Usually by hydrolysis
• “splitting with water”
• Adds H2O back into molecule
• Breaks covalent bonds
Cellular Metabolism
• Catabolism
• Energy is released when bonds
break
• Reverse of dehydration synthesis
(condensation)
• Hydrolysis = chemical digestion
• Occurs simultaneously (and
continuously) with anabolism
• Processes controlled by enzymes
•
Cellular Energy
• Cellular energy is chemical energy
• Derived from breaking chemical
bonds
• ~ ½ Energy is stored as ATP
• ~ ½ Energy is released as heat
• Helps maintain body
temperature
• Enzymes control in the process
Cellular Energy
All nutrient molecules are ultimately
degraded or converted to glucose
Only glucose can be used to make
ATP
Oxidation: cellular process of
chemically breaking apart a
glucose molecule to release
energy
Cellular Energy
Glucose oxidation occurs in 2
phases
Anerobic metabolism
Occurs in cytoplasm
Without oxygen
AKA glycolysis
Splits glucose into two 3-Carbon
molecules: pyruvate
Cellular Energy
Glycolysis
Process also produces 2 ATPs
In yeast, plant cells:
Pyruvate can undergo alcoholic
fermentation
In bacteria, animal cells:
Pyruvate can produce lactic acid
Cellular Energy
Aerobic metabolism
Uses oxygen
AKA Kreb’s Cycle or Citric Acid
cycle or Tricarboxylic Acid (TCA)
Cycle
Occurs in mitochondria
Makes more ATP than anerobic
processes
Cellular Energy
Aerobic metabolism
CO2 and H2O are waste products
CO2:
Diffuses out of cells
Dissolves in plasma
Produces HCO3- in blood
Exhaled from lungs
Cellular Energy
Aerobic metabolism
H2O:
“metabolic” water
Exhaled from lungs
Final products of glucose oxidation:
CO2, H2O, ATP
Cellular Energy
Aerobic metabolism
For each molecule of glucose:
2 ATP formed in glycolysis
36 ATP formed in TCA cycle
Energy stored in phosphate bonds
A reversible reaction
Metabolic Pathways
“A particular sequence of enzymatic
reactions”
Such as glycolysis, TCA cycle
Carbohydrate pathways
Carbos should comprise most of
our diet (~ 50% complex carbs)
Used as a primary energy source
Produce 4kcal/gm
Metabolic Pathways
Carbohydrate pathways
Excess carbs converted to energy
storage forms
Glycogen (muscle, liver)
Adipose tissue (hips)
Process is anabolism
Metabolic Pathways
Lipid pathways
Metabolism controlled by liver
Should comprise <30% of calories
in diet
Get 9 kcal/gm (more ATP!)
Must be degraded into glycerol,
fatty acids, then pyruvate
A reversible catabolic process
Metabolic Pathways
Protein pathways
Proteins should comprise ~30% of
diet
Get 4 kcal/gm
Catabolism is more complex
Proteins contain nitrogen
Metabolic Pathways
Protein pathways
Deamination: removal of nitrogen
from amino acids
Occurs in liver
Nitrogen is converted to urea
A nitrogenous waste product
Sent to kidneys for excretion
Metabolic Pathways
Protein pathways
After deamination:
amino acid “skeleton” is processed
in TCA cycle
May produce CO2, H2O, ATP
May form glucose or fat
Metabolic Pathways
Protein pathways
Glucose formed from amino acid
skeletons may be re-converted to
amino acids
“Essential” amino acids:
Body cannot make these
Must obtain in the diet
Regulation of Metabolic
Pathways
Enzyme “saturation”
Too much substrate for number of
enzyme molecules
Reaction rate cannot increase
A single enzyme can control an
entire metabolic pathway
“rate limiting” enzyme
Digestive System: Disorders
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14.92b
Digestive System: Disorders
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14.92b
Review !!!!!
Activation of Pepsin
HCl
Digests
Parietal Protein
Cell
STIMULATION OF GASTRIC
SECRETION: Cephalic Phase
Seeing, Vagus Intrinsic Nerves Parietal
Smelling, & Chief
Tasting Pyloric Area Cells
Food
Increased
Gastrin Gastric
Secretion
STIMULATION OF GASTRIC
SECRETION: Gastric Phase
Stimuli Intrinsic Nerves Parietal
in Stomach: Vagus & Chief
protein, Pyloric Area Cells
distension,
caffeine,
alcohol
Increased
Gastrin Gastric
Secretion
THE GASTRIC MUCOSAL
BARRIER
• Protects the cells from contents of
stomach
• Luminal membranes of cells are
impermeable to protons
• Cells are tightly adjoined
• Rapid turnover
• If broken, peptic ulcer may result: positive
feedback involving histamine
Gastrin secretion inhibition
• Acid in antrum
•
• removal of protein as stomach empties
PANCREATIC AND BILLIARY
SECRETIONS
• THE PANCREAS IS BOTH ENDOCRINE AND
EXOCRINE
• THE EXOCRINE PANCREAS SECRETES DIGESTIVE
ENZYMES AND AN AQUEOUS ALKALINE FLUID
• PANCREATIC SECRETION IS HORMONALLY
REGULATED
• PANCREATIC SECRETIONS REACH THE SMALL
INTESTINE VIA THE COMMON BILE DUCT
THE EXOCRINE PANCREAS
SECRETES DIGESTIVE ENZYMES
• PROTEOLYTIC ENZYMES
• PANCREATIC AMYLASE
• PANCREATIC LIPASE
HORMONAL CONTROL OF
PANCREATIC SECRETION
• ACID IN DUODENAL LUMEN >SECRETIN:
STIMULATES PANCREATIC DUCT CELLS
TO PRODUCE SIGNIFICANT QUANTITES
OF AQUEOUS ALKALINE SECRETION
• FAT AND PROTEIN IN DUODENAL
LUMEN>CHOLECYSTOKININ
(CCK):STIMULATES PANCREATIC ACINAR
CELLS TO SECRETE DIGESTIVE ENZYMES
FUNCTIONS OF THE LIVER
• METABILIC PROCESSING OF ABSORBED
FOOD
• DETOXIFICATION2
• SYNTHESIS OF PLASMA PROTEINS
• STORAGE OF GLYCOGEN AND FAT, ETC.
• REMOVAL OF BACTERIA AND WORN-OUT
RBC
• EXCRETION OF CHOLESTEROL AND
BILIRUBIN
•
BILE SECRETION, STORAGE,
AND CIRCULATION
• SECRETED BY THE LIVER
• RECYCLED THROUGH
ENTEROHEPATIC CIRCULATION
• STORED IN GALL BLADDER
LIVER BLOOD FLOW
INFERIOR
VENA CAVA AORTA
HEART
HEPATIC HEPATIC
VEIN ARTERY
LIVER
HEPATIC
PORTAL ARTERIES TO
VEIN DIGESTIVE TRACT
STOMACH
AND
SMALL
INTESTINE
BILE SALT CIRCULATION
LIVER
GALL BLADDER
SPHINCTER
OF ODDI
DUODENUM
S.I. MOTILITY
• SEGMENTATION CONTRACTIONS
•
• PACEMAKER CELLS
•
• MIXING AND PROPULSION
SEGMENTATION
CONTRACTIONS
Lumen
Cells
Plasma
Sodium Absorption
PUMP: Na/K ATPase
Lumen Sodium
Cells
Potassium
Plasma
Chloride
Water
AVERAGE DAILY INTAKE OF IRON
(NORTH AMERICA AND EUROPE)
• BETWEEN 10 AND 30 mg
• ABOUT 5 TO 7 mg PER 1000 CALORIES
• IF ON A 1000 TO 1500 CALORIE DIET,
ONLY 6-9 mg
• INFLUENCED BY COOKING UTENSILS
• DEPENDS ON BEVERAGE
CONSUMPTION
THE LARGE INTESTINE
• PRIMARILY A DRYING AND STORAGE
ORGAN
• HAUSTRAL CONTRACTIONS
• MASS MOVEMENTS
• PROTECTIVE SECRETIONS
• FORMATION OF FECES
THE DEFICATION REFLEX
• DISTENTION OF RECTUM STIMULATES
• INTERNAL ANAL SPHINCTER (SMOOTH
MUSCLE) RELAXES
• EXTERNAL ANAL SPHINCTER
(SKELETAL MUSCLE) UNDER
VOLUNTARY CONTROL
GASTROINTESTINAL
HORMONES
• GASTRIN
• SECRETIN
• CHOLECYSTOKININ
GASTRIN
• ENDOCRINE CELLS IN PYLORIC STOMACH
• STIMULATED BY PROTEIN IN STOMACH
• STIMULATES SECRETION BY PARIETAL AND
CHIEF CELLS
• STIMULATES ILEAL MOTILITY
• RELAXES ILEOCECAL SPHINCTER
• INDUCES COLONIC MASS MOVEMENTS
SECRETIN
• ENDOCRINE CELLS IN DUODENAL MUCOSA
• ACID IN DUODENAL LUMEN
• INHIBITS GASTRIC EMPTYING
• INHIBITS GASTRIC SECRETION
• STIMULATES AQUEOUS BICARBONATE SECRETION
BY PANCREAS
• STIMULATES BICARBONATE RICH BILE SECRETION
BYLIVER
•
CHOLECYSTOKININ
• ENDOCRINE CELLS IN DUODENAL MUCOSA
• FAT AND PROTEIN IN DUODENAL LUMEN
• INHIBITS GASTRIC EMPTYING
• INHIBITS GASTRIC SECRETION
• CAUSES GALL BLADDER CONTRACTION
• CAUSES RELAXATION OF THE SPHINCTER OF ODDI
• CONTRIBUTES TO SATIETY
TOTAL BODY IRON IN
HUMANS
• WEIGHT
• SEX
• SIZE OF STORAGE COMPARTMENT
• HEMOGLOBIN CONCENTRATION
• HISTORY
ABSORPTION OF IRON FROM
FOODS
FOOD DOSE (mg) % ABSORBED
RICE 2 1
SPINACH 2 2-3
LETTUCE 17 3-5
WHEAT 2-4 5
VEAL 3 10-18
LIVER
• CANCER
• HEART DISEASE
• HIGH BLOOD PRESSURE
• OBESITY
• DIVERTICULITIS
FOOD INGREDIENTS AND DISEASE
• REFINED SUGAR
• FAT
• SALT
• LOW IN FIBER
CANCER AND DIET: PHYTOCHEMICALS
• SOYBEANS
•
• QUINONA
•
• SPINACH
•
• HAVE THE SAME QUALITY AS MILK
INCOMPLETE PROTEINS NEEDED TO MEET
REQUIREMENTS
• SOLUABLE • INSOLUABLE
• SOME • LIGNIN
HEMICELLULOSE • CELLULOSE
• PECTIN • SOME
• GUM HEMICELLULOSE
• MUCILAGES
CHELATORS LOWER MINERAL ABSORPTION
• PHYTATES
•
• OXALATES
SUPPLIMENTS FROM PLANTS
• ECHINACEA: IMMUNE BOOSTING AND ANTIBIOTIC
• PSYLLIUM SEEDS: SOURCE OF FIBER
• CHAMOMILE: MILD SEDATIVE
• ALOE VERA: PROMOTES HEALING
• SAW PALMETTO EXTRACT: PROSTATE PROBLEMS
• GREEN TEA: ANTI CANCER , ANTIOXIDENT
• GARLIC: ANTIBACTERIAL, ANTIVIRAL, LOWERS
CHOLESTEROL
Chapter 18
The Digestive
System
Functions of the GI Tract
§ Motility:
Movement of of food through the GI tract.
Ingestion:
Taking food into the mouth.
Mastication:
Chewing the food and mixing it with saliva.
Deglutition:
Swallowing the food.
Peristalsis:
Rhythmic wave-like contractions that move food
through GI tract.
Functions of the GI Tract (continued)
Secretion:
Digestion:
Breakdown of food particles into subunits
(chemical structure change).
Absorption:
Process of the passage of digestion
(chemical subunits) into the blood or
lymph.
Storage and elimination:
Temporary storage and elimination of
indigestible food.
Digestive System (GI)
GI tract divided
Insert fig. 18.2
into:
Alimentary
canal.
Accessory
digestive
organs.
GI tract is 30 ft
long and
extends from
mouth to anus.
Layers of GI Tract
Composed of 4
tunics:
Mucosa.
Submucosa.
nMuscularis.
nSerosa.
Mucosa
Secrete mucus.
Submucosa
lymphatic vessels.
Submucosal plexus (Meissner’s plexus):
layers.
Major nerve supply to GI tract.
Extrinsic innervation:
activity.
Regulation of the GI Tract (continued)
Mastication (chewing):
Peristalsis:
contractions:
Circular smooth
muscle contract
behind, relaxes in
front of the bolus.
Followed by
longitudinal
contraction
(shortening) of
smooth muscle.
Rate of 2-4 cm/sec.
Stomach
Stores food.
Kills bacteria.
Contractions of
the stomach
churn chyme. Insert fig. 18.5
Mix
chyme
with
gastric
secretio
ns.
Push food
into
intestin
e.
Stomach (continued)
• Gastric mucosa
has gastric Insert fig. 18.7
pits in the
folds.
• Cells that line
the folds
deeper in the
mucosa, are
gastric
glands.
Gastric Glands
• Parietal cells
secrete H+ into
gastric lumen
by primary Insert fig. 18.8
active
transport,
through H+/ K+
ATPase pump.
• Parietal cell’s
basolateral
membrane
takes in Cl-
against its
electrochemica
l gradient, by
coupling its
transport with
HC03-.
HCl Production (continued)
Indirectly by gastrin.
Indirectly by ACh.
ACh and gastrin stimulate release of
histamine.
Histamine:
Stimulates parietal cells to secrete HCl.
HCl Functions
pepsinogen to
pepsin.
Pepsin is more
active at pH
of 2.0.
Digestion and Absorption in the
Stomach
Peptic ulcers:
2 major types of
paced by graded
depolarizations called
slow waves.
Slow waves
produced by
interstitial cells of
Cajal.
Slow waves spread
from 1 smooth
muscle cell to
Contractions of Intestinal Smooth
Muscles
lumen.
Guanylin stimulates secretion of Cl- and H20, and
inhibits absorption of Na+ (minor pathway).
Membrane contains Na+/K+ pumps.
Minor pathway.
Fluid and Electrolyte Absorption in
the Intestine
Small intestine:
by bile ducts.
Structure of Liver (continued)
Compounds that
recirculate between
liver and intestine.
Many compounds Insert fig. 18.22
can be absorbed
through small
intestine and
enter hepatic
portal blood.
Variety of
exogenous
compounds are
secreted by the
liver into the bile
ducts.
Can excrete these
Major Categories of Liver Function
Bile Production and Secretion
conjugated bilirubin.
Secreted into bile.
Converted by bacteria in intestine to urobilinogen.
cholesterol.
Major pathway of Insert fig. 18.25
cholesterol
breakdown in the
body.
Principal bile acids are:
Cholic acid.
Chenodeoxycholic
acid.
Combine with glycine
or taurine to form
bile salts.
Bile salts
aggregate as
micelles.
Detoxification of the Blood
drugs.
Conjugation of steroid hormones and
xenobiotics make them anionic.
Can be transported into bile by multispecific
organic anion transport carriers.
Steroid and xenobiotic receptors stimulate
production of cytochrome P450
enzymes.
Secretion of Glucose, Triglycerides
and Ketones
Liver helps regulate blood glucose
concentration by:
Glycogenesis and lipogenesis.
Glycogenolysis and gluconeogenesis.
Contains enzymes required to convert free
closes.
Bile is forced up to the cystic duct to gallbladder.
Pancreas
Exocrine:
Insert fig. 18.26
Acini:
Secrete
pancre
atic
juice.
Endocrine:
Islets of
Langerha
ns:
Secrete
insulin
and
glucag
on.
Pancreatic Juice
into 3 phases:
Cephalic phase.
Gastric phase.
Intestinal phase.
Cephalic Phase
Stimulated by sight, smell, and taste of food.
Activation of vagus:
pepsinogen.
Directly stimulates G cells to secrete
gastrin.
Directly stimulates ECL cells to secrete
histamine.
Indirectly stimulates parietal cells to
secrete HCl.
Continues into the 1st 30 min. of a meal.
Gastric Phase
Arrival of food in stomach stimulates the gastric phase.
Gastric secretion stimulated by:
Distension.
Chemical nature of chyme (amino acids and short
polypeptides).
Stimulates G cells to secrete gastrin.
Stimulates chief cells to secrete pepsinogen.
Stimulates ECL cells to secrete histamine.
Histamine stimulates secretin of HCl.
Positive feedback effect.
As more HCl and pepsinogen are secreted, more
polypeptides and amino acids are released.
Gastric Phase (continued)
regulated by a
negative feedback
effect:
Insert. Fig. 18.30
HCl secretion
decreases if pH
< 2.5.
At pH of 1.0,
gastrin secretion
ceases.
D cells
stimulate
secretion of
somatostatin
.
Paracrin
e
Intestinal Phase
Inhibits gastric activity when chyme enters the
small intestine.
Arrival of chyme increases osmolality and
distension.
Activates sensory neurons of vagus and produces
an inhibitory neural reflex:
Inhibits gastric motility and secretion.
In the presence of fat, enterogasterone inhibits gastric
motility and secretion.
Hormone secretion:
• Peristalsis:
• ACh and
substance P Insert fig. 18.31
stimulate
smooth
muscle
contraction
above the
bolus.
• NO, VIP, and
ATP stimulate
smooth
muscle
relaxation
Paracrine Regulators of the Intestine
Serotonin (5-HT):
Begins starch
Insert fig. 18.32
digestion.
Pancreatic amylase:
Digests starch to
oligosaccharides.
Oligosaccharides
hydrolyzed by
brush border
enzymes.
Glucose is transported
by secondary active
transport with Na+ into
the capillaries.
Digestion and Absorption of Protein
Chymotrypsin.
Elastase.
Aminopeptidase.
Digestion and Absorption of Protein
(continued)
the liver.
Form VLDLs which take triglycerides to cells.
Once triglycerides are removed, VLDLs are
converted to LDLs.
LDLs transport cholesterol to organs and blood
vessels.
HDLs transport excess cholesterol back to liver.
Absorption of Fat
• Heart – ANP
•
• Placenta - hCG
Endocrine
System
Function
• Maintenance of homeostasis
through negative feedback
loops
Endocrine System Function
cholesterol (lipid)
acid
Steroid Hormones
Mainly from the adrenal cortex and/or
gonads
Mineralocoritcoid → aldosterone
Glucocorticoids → cortisol, cortisone
Sex steroids → progestin, estrogens,
androgens
Non-steroid Hormones
• Example: prostaglandins
•
Pituitary
Note:
1.GH is also called somatotropin
2.There are also inhibitory factors from the hypothalamus for G
Posterior Pituitary
• GHRH/somatostatin GH or
somatotropin cells related to body
growth
•
In men
increases sensitivity to LH and indirectly
enhances testosterone production
Thyroid
Gland
• 2 lobes, on either
side of the
trachea,
connected by
an isthmus
Microscopic
Thyroid Gland
anatomy
• Thyroid follicles,
lined by secretory
epithelium
(follicular cells)
•
• Filled with
thyroglobulin
(transport protein)
•
• Parafollicular cells
between the
follicles
Thyroid
Function
• Secretes two
hormones
(both require
iodine as a
precursor)
•
• Less active
•
• Converted to T3 in
the cell
•
• Most remains in
the bloodstream
as reservoir of
thyroid hormone
Thyroid Function
In adults
glycogenolysis
gluconeogenesis
Adrenal Cortex
3
layer
s
Adrenal Cortex
Zona mineralocorticoidsAldosterone:
Glomerulosa renal Na+ & water
Zona gluccorticoids reabsorption
Cortisol
Fasciculata
1.
Adrenal Cortex: Z. Fasciculata
Potential electrolyte
imbalance (Aldosterone)
Mood changes
(Testosterone)
Gonads
Ovaries Testes
Stimulates mineral
deposition in bone by
osteoblasts
Pancreas
• Not linked to hypothalamic
pituitary axis
• Both exocrine & endocrine
functions
Pancreas
• Endocrine hormones: insulin & glucagon
secreted by cells in the islets of
Langerhans
•
Glucagon
•Except
CNS...does not
require insulin
to take up
glucose
Diabetes Mellitus
• Elevated blood sugar
•
Polydipsia (thirst)
Polyphagia (hunger)
membranes to insulin
NIDDM (Non Insulin Dependent DM)
usually does not require insulin (oral
hypoglycemics)
Usually onset is as an adult
Onset is insidious
Usually no ketoacidosis
Diabetes Mellitus
• Long term monitoring of blood sugar
levels (months)
•
• Larger in
adolescence
•
• Regresses at
puberty
•
• Secretes thymosin
•
Thymus
cortex
medulla
• An immediate response
•
consumed:
Hypothalamus → CRH
→ ACTH → Cortisol
Stress: The Resistance Phase
•
Stress: The Exhaustion Phase
• Eicosanoids are
paracrine
secretions
•
• They are
produced by the
Arachidonic
acid pathway
Arachidonic Acid Pathway
• Arachidonic acid
(a fatty acid) is
produced from
phospholipids
in the cell
membrane
•
• This reaction is
catalyzed by
phospholipase
A2
Arachidonic Acid Pathway
Arachidonic acid is
then subjected to
either of two
metabolic
pathways
1.lipoxygenase –
leads to the
production of
leukotrienes,
chemical
mediators of
inflammation
Arachidonic Acid Pathway
2.cyclooxygenase
– leads to the
production of
prostaglandin
s,
thromboxane,
and
prostacyclin
Paracrine Secretions
Thromboxane is secreted by platelets to
enhance platelet aggregation
Dennis N. Muñoz,
Muñoz PT, RN,RM
Urinary System
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 2.1
General Information
•Waste products of metabolism are
toxic (CO2 , ammonia, etc.)
•Removal from tissues:
•by blood and lymph
•Removal from blood by:
•Respiratory system
•Urinary system
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.1a
Functions of the Urinary
System
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.1a
Functions of the Urinary
System
•Regulate homeostasis
•Water balance
•Electrolytes
•Acid-base balance in the blood
•Blood pressure
•Red blood cell production
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.1b
Organs of the Urinary system
•Kidneys
•Ureters
•Urinary bladder
•Urethra
Figure 15.1a
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.2
Location of the Kidneys
•Retroperitoneally
•Lateral to vertebral column
•The right kidney is slightly lower
than the left
•Atop each kidney is an adrenal gland
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.3
Organs of the Urinary system
•Kidneys
•
Figure 15.1a
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.2
Structure of the Kidney
Outer cortex:
Contains
many
capillaries.
Medulla:
Renal
pyramids
separated
by renal
columns.
Pyramid
contains
n minor
Major calyces form renal pelvis.
calyces
n Renal pelvis collects urine.
which
n Transports urine to ureters.
unite to
Coverings of the Kidneys
•Renal capsule
•Surrounds each kidney
•Adipose capsule
•Surrounds the kidneys
•Provides protection to the kidneys
•Helps hold kidneys in place
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.4
Regions of the Kidney
•Renal cortex:
outer region
•Renal medulla:
pyramids and
columns
•Renal pelvis:
collecting system
Figure 15.2b
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.5
Kidney Structures
•Medullary pyramids – triangular
regions of tissue
•Renal columns– cortical material
between pyramids
•Calyces (sing. Calyx)
•cup-shaped structures
•collect urine
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.6
Structures involved in Urine
•Vascular
Formation Components
•Afferent arteriole
•Glomerulus
•Efferent arteriole
•Peritubular capillaries
•Tubular Components
•Bowman’s capsule
•Proximal convoluted tubule
•Loop of Henle
•Distal convoluted tubule
•
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.6
Blood Flow
in/to the
Kidneys
•Is extensive!!!
Figure 15.2c
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.7
Renal Blood Vessels (continued)
Afferent arteriole:
Blood
vessels:
Vasa recta.
Peritubular
capillaries.
Urinary
tubules:
PCT.
LH.
DCT.
Type of Nephrons
Cortical nephron:
Originates in
outer 2/3 of
cortex. Insert fig. 17.6
Osmolarity of
300 mOsm/l.
Involved in
solute
reabsorption.
Juxtamedullary
nephron:
Originates in
inner 1/3
cortex.
Nephrons Review !!!!
•The structural and functional units
of the kidneys
•Responsible for forming urine
•Components of the nephrons
•Renal corpuscle
•Glomerulus and Bowman’s capsule
•Renal tubules
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.8
Glomerular Capsule
Bowman’s
capsule:
Surrounds
Insert fig. 17.6
the
glomerulu
s.
Location
where
glomerul
ar
filtration
occurs.
Proximal Convoluted Tubule
Loop of Henle
Distal Convoluted Tubule
Glomerulus (“a ball of yarn”)
•A specialized
capillary bed
•Attached to
arterioles on both
sides
•Wide afferent
arteriole
•Narrow efferent
arteriole
Figure 15.3c
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.9a
Glomerulus
•Covered by
glomerular
capsule
•first part of
the renal
tubule
•AKA Bowman’s
capsule
Figure 15.3c
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.9b
Renal Tubule
•Bowman’s
capsule
•Proximal
convoluted
tubule
•(PCT)
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 15.3b Slide 15.10
Renal Tubule
•Loop of Henle
•Distal
convoluted
tubule
•DCT
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 15.3b Slide 15.10
Peritubular Capillaries
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.12
Renal Tubule
•Peritubular
capillaries
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Figure 15.3b Slide 15.10
Glomerular Filtration Membrane
Glomerular Filtration Membrane (continued)
Stimulates
vasoconstriction of
afferent arterioles. Insert fig. 17.11
Preserves blood
volume to muscles
and heart.
Cardiovascular
shock:
Decreases
glomerular
capillary
hydrostatic
Renal Autoregulation of GFR
Ability of kidney to maintain a constant GFR
under systemic changes.
Achieved through effects of locally produced
chemicals on the afferent arterioles.
When MAP drops to 70 mm Hg, afferent
arteriole dilates.
When MAP increases, vasoconstrict afferent
arterioles.
Tubuloglomerular feedback:
•Filtration
•Reabsorption
•Secretion
Figure 15.4
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.13
Filtration
•Nonselective passive process
•Depends on hydrostatic pressure
•Stops if B.P. falls too low
•Water and some solutes (no proteins)
•forced through capillary walls
•Taken out of blood
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.14
Filtration
•Blood cells cannot pass
•Filtrate is collected in the
glomerular capsule
•This will become urine
•Leaves capsule through the renal
tubule
•Alterations to filtrate occur in
tubule
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.14
Reabsorption
•Moving reusable material back into the
blood
•The peritubular capillaries reabsorb
several materials
•Some water
•Glucose
•Amino acids
•Ions
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.15
Reabsorption, con’t…
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.15
Reabsorption, con’t…
•Loop of Henle
•15% more filtrate reabsorbed
•Descending limb:
•Water, by osmosis
•Ascending limb:
•Cl- by active transport
•Na+ by diffusion
•
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.15
REMEMBER!!!!
Reabsorption of Salt and H20
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.16
Reabsorption in Proximal Tubule
Na+/K+ ATPase pump located in basal
and lateral sides of cell membrane,
creates gradient for diffusion of Na+
across the apical membrane.
Na+/K+ ATPase pump extrudes Na+.
• NaCl is actively
extruded Insert fig. 17.15
from the
ascending
limb into
surrounding
interstitial
fluid.
• Na+ diffuses
into tubular
cell with the
secondary
active
Ascending Limb LH (continued)
• Na+ actively
transported
across the Insert fig. 17.15
basolateral
membrane by
Na+/ K+
ATPase
pump.
• Cl- passively
follows Na+
down
electrical
gradient.
Descending Limb LH
• Deeper regions of
medulla reach 1400 Insert fig. 17.16
mOsm/L.
• Impermeable to
passive diffusion of
NaCl.
• Permeable to H20.
• Hypertonic interstitial
fluid causes H20
movement out of
the descending limb
via osmosis, and
Countercurrent Multiplier System
Multiplies the
[interstitial fluid] Insert fig. 17.16
and [descending
limb fluid].
Flow in opposite
directions in the
ascending and
descending
limbs.
Close proximity of
the 2 limbs:
Allows
Vasa Recta
Countercurrent
exchange.
Recycles NaCl in Insert fig. 17.17
medulla.
Transports H 0 from
2
interstitial fluid.
Descending limb:
Urea transporters.
Aquaporin proteins
(H20 channels).
Ascending limb:
Fenestrated
Vasa Recta (continued)
LH and terminal
CD are
permeable to
urea.
Terminal CD
has urea
transporters.
Collecting Duct
Medullary area impermeable to high [NaCl]
presence of ADH.
When ADH binds to its membrane
receptors on CD, it acts via cAMP.
Stimulates fusion of vesicles with plasma membrane.
Incorporates water channels into plasma membrane.
Secretion: Reabsorption in
Reverse
•Some materials move from peritubular
capillaries into renal tubules
•Hydrogen and potassium ions
•Creatinine
•Most secretion occurs in DCT
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.17
Secretion: Reabsorption in
Reverse
•What’s left?? Urine!
•Moving urine out of kidneys:
tubules
collecting duct
minor calyces
major calyces
renal pelvis
ureter
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.17
Secretion
Secretion of substances from the peritubular
capillaries into interstitial fluid.
Then transported into lumen of tubule, and into
the urine.
Allows the kidneys to rapidly eliminate certain
potential toxins.
Proximal Tubule
Insert fig. 17.13
Secretion
Transport Process Affecting Renal Clearance
Ability of the kidneys to remove
molecules from plasma and excrete
those molecules in the urine.
If a substance is not reabsorbed or
secreted by tubule:
The amount excreted in urine/min. will be
equal to the amount filtered out of the
glomeruli/min.
Rate at which a substance is filtered by
the glomeruli can be calculated:
Quantity filtered = GFR x P
P = inulin concentration in plasma.
Amount filtered = amount excreted
GFR = V x U
Renal Clearance of Inulin
• 45% blood
is RBCs
Insert fig. 17.23
• 55%
plasma
• Total renal
blood
flow =
PAH
clearance
0.55
Glucose and Amino Acid Reabsorption
Filtered glucose and amino acids are
normally reabsorbed by the nephrons.
In PCT occurs by secondary active
transport with membrane carriers.
Carrier mediated transport displays:
Saturation.
Tm.
[Transported molecules] needed to saturate carriers
and achieve maximum transport rate.
Renal transport threshold:
Minimum plasma [substance] that results in
excretion of that substance in the urine.
Renal plasma threshold for glucose = 180-200
mg/dl.
Electrolyte Balance
Kidneys regulate Na+, K+, H+, Cl-, HC03-,
and PO4-3 .
Control of plasma Na+ is important in
90% filtered K+ is reabsorbed in early part of
the nephron.
Secretion of K+ occurs in CD.
Amount of K+ secreted depends upon:
Amount of Na+ delivered to the region.
Amount of aldosterone secreted.
As Na+is reabsorbed, lumen of tubule becomes
–charged.
Potential difference drives secretion of K+ into tubule.
Transport carriers for Na+ separate from transporters for
K+.
DUAL CONTROL OF ALDOSTERONE
SECRETION
Fall in sodium
Increased ECF Volume
Plasma
Potassium Blood Pressure
Increased Urinary
Potassium Secretion Fall in Urinary
Sodium Excretion
K+ Secretion (continued)
Final [K+]
controlled in
CD by Insert fig. 17.24
aldosterone.
When
aldosterone
is absent,
no K+ is
excreted in
the urine.
High [K+] or low
[Na+]
stimulates the
secretion of
Juxtaglomerular Apparatus
secrete renin:
Converts angiotensinogen to angiotensin I.
Initiates the renin-angiotensin-aldosterone system.
Negative feedback.
Macula densa:
Region where ascending limb is in contact with
afferent arteriole.
Inhibits renin secretion when blood [Na+] in blood
Juxtaglomerular Apparatus (continued)
Figure 15.5
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.18
Acidification of Urine
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.19
Normal volume of Urine
•0.6 – 2.5 liters/day. Depends on:
•Adequate B.P.
•Fluid intake
•Temperature, humidity
•Activity levels
•<30cc/hour output = kidney
failure
•Average is 115-125 ml/hr
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.19
Abnormal components of Urine
•Glucose
•Ketones
•Hemoglobin/blood cells
•Proteins
•pH <4 or >8
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.19
Ureters
•Tubes attaching kidney to urinary
bladder
•Continuous with the renal pelvis
•Enter the posterior aspect of the
bladder
•Retroperitoneal
•Peristalsis, gravity move urine
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.20
Essentials of Anatomy and
Physiology
Fifth edition
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 2.1
Urinary Bladder
•Smooth, collapsible, muscular sac
•Temporarily stores urine
Figure 15.6
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.21a
Urinary Bladder
•Trigone – three openings
•Two from the ureters
•One to the urethra
Figure 15.6
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.21b
Urinary Bladder Wall
•Three layers of smooth muscle
(detrusor muscle)
•Mucosa made of transitional
epithelium
•Walls are thick and folded
•If bladder is empty
•Bladder can expand significantly
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.22
Urethra
•Thin-walled tube that
•carries to the outside of the
body
•by peristalsis
•Release of urine is controlled by:
•Internal urethral sphincter
(involuntary)
•External urethral sphincter
(voluntary)
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.23
Urethra
• Release of urine
is controlled by:
• Internal
urethral
sphincter
(involuntar
y)
• External
urethral
sphincter
(voluntary)
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
Urethra: Gender Differences
•Length
•Females – 3–4 cm (1 inch)
•Males – 20 cm (8 inches)
•Location
•Females – anterior to the vagina
•Males – through the prostate and
penis
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.24a
Urethra: Gender Differences
•Function
•Females – only carries urine
•Males – carries urine and semen
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.24b
Micturition (Voiding)
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.25
Micturition Reflex
Actions of the internal urethral sphincter and the
external urethral sphincter are regulated by
reflex control center located in the spinal cord.
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.26
Distribution of Body Fluid
•Intracellular
fluid (inside
cells)
•Extracellular
fluid (outside
cells)
•Interstitial
fluid
•Blood plasma
Figure 15.7
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.27
The Link Between Water and
Salt
•Changes in electrolyte balance
causes water to move from one
compartment to another
•Alters blood volume and blood
pressure
•Can impair the activity of cells
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.28
Maintaining Water Balance
•Water intake must equal water output
•Intake
•Ingested foods and fluids
•Water produced from metabolic processes
•Output
•Lungs
•Perspiration
•Feces
•Urine production
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.29
Maintaining Water Balance
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.30
Regulation of Water and
Electrolyte Reabsorption
•Regulation is primarily by hormones
•Antidiuretic hormone (ADH) prevents
excessive water loss in urine
•Aldosterone regulates sodium ion
content of extracellular fluid
•Cells in the kidneys and hypothalamus
are active monitors
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.31
Regulation of Water and
Electrolyte Balance
•Primarily by hormones
•Antidiuretic hormone (ADH): prevents
excessive water loss
•Aldosterone: regulates sodium ion
content ECF
•Monitored by cells in kidneys and
hypothalamus
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.31
Maintaining Acid-Base Balance
in Blood
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.33b
Renal Mechanisms of Acid-
Base Balance
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.37
Effects of Aging on the Urinary
System: FYI
•There is a progressive decline in
urinary function
•Output decreases ~1cc/yr >50
•The bladder shrinks with aging
•Urinary retention is common in males
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.39
Disorders of the Urinary System:
FYI
•Nephritis: inflammation of nephrons
•Protein appears in urine
•Kidney stones
•More common in males
•Glucosuria
•Sugar in urine: diet or diabetes??
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.39
Disorders of the Urinary System:
FYI
•Cystitis
•Bacterial infection of urinary
bladder
•Gout
•Genetic. Uric acid crystals
ppct in joints
•Non-gonococcal urethritis (NGU)
•A sexually transmitted infection
Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Slide 15.39
Renal Failure
THE URINARY BLADDER STORES THE
URINE
Reflex and Voluntary Control of
Micturition
1052
05/24/2010
1053
WATER STEADY STATE 05/24/2010
• Pathological losses
üvascular bleeding (H20,
Na+)
üvomiting (H20, H+)
üdiarrhea (H20, HCO3-).
1054
05/24/2010
1055
05/24/2010
ELECTROLYTE LOSSES
1056
05/24/2010
BODY FLUIDS
Functions of Fluids
qBody fluids:
üFacilitate in the transport
[nutrients, hormones, proteins,
& others…]
üAid in removal of cellular
metabolic wastes
üProvide medium for cellular
metabolism
üRegulate body temperature
üProvide lubrication of
musculoskeletal jts. 1057
05/24/2010
REVIEW OF FUNCTIONS OF
WATER IN THE BODY
• Transporting nutrients to cells and wastes from cells
• Transporting hormones, enzymes, blood platelets, and
red and white blood cells
• Facilitating cellular metabolism and proper cellular
chemical functioning
• Acting as a solvent for electrolytes and nonelectrolytes
• Helping maintain normal body temperature
• Facilitating digestion and promoting elimination
• Acting as a tissue lubricant
1058
BODY WATER DISTRIBUTION
•Individual variability (lean body mass)
–55 - 60% of body weight in adult males Input
–50 - 55% of body weight in adult female
–~42 L For a 70 Kg man.
TRANSCELLULAR WATER
05/24/2010 1% 1 L 1059
05/24/2010
ELECTROCHEMICAL EQUIVALENCE
1060
05/24/2010
(30%)
Includes intravascular and interstitial fluids
1061
05/24/2010
water
Women and obese people have less body
water
1062
05/24/2010
1063
05/24/2010
1064
05/24/2010
OSMOLARITY OF A SOLUTION
1065
05/24/2010
FILTRATION
• Colloid osmotic pressure
• Hydrostatic pressure
1066
05/24/2010
1067
05/24/2010
Figure 26.4
1068
05/24/2010
FLUID LOSSES
• Kidneys — urine
• Intestinal tract — feces
• Skin — perspiration
• Insensible water loss
1069
05/24/2010
1070
05/24/2010
PRIMARY ORGANS OF
HOMEOSTASIS
Kidneys normally filter 170 L plasma, excrete 15
L urine
Cardiovascular system pumps and carries
nutrients and water in body
Lungs regulate oxygen and carbon dioxide
levels of blood
Adrenal glands help body conserve sodium,
save chloride and water, and excrete
potassium
Thyroid gland increases blood flow in body and
increases renal circulation
1071
05/24/2010
PRIMARY ORGANS OF
HOMEOSTASIS (CONT.)
• Parathyroid glands regulate the level of
calcium in ECF
• GI tract absorbs water and nutrients that
enter body though this route
• Nervous system is a switchboard to inhibit
and stimulate fluid balance (thirst center
and ADH storage)
1072
05/24/2010
QUESTION
ANSWER
Answer: A. True
A hypertonic solution has a greater
osmolarity, causing water to move out of
the cells and to be drawn into the
intravascular compartment, causing the
cell to shrink.
1074
05/24/2010
BODY FLUIDS
3 9
L L
40 % TBW 20 % TBW
1075
05/24/2010
BODY FLUIDS
1076
05/24/2010
ICF ECF
Capillary P (Hydrostatic P)
P ISF
1077
05/24/2010
OBLIGATORY Reabsorption
qoccurs in the proximal tubules
q178 L/day of glomerular filtrate (80%
reabsorbed)
q2 to solute reabsorption
qindependent of the water requirement
FACULTATIVE Reabsorption
qoccurs in the distal & collecting tubules
qindependent of the active solute
transport
qdependent of body’s need of water 1078
05/24/2010
1079
05/24/2010
1080
05/24/2010
Figure 26.5
1081
05/24/2010
1082
05/24/2010
1083
05/24/2010
Figure 26.6
1084
05/24/2010
EDEMA (Dropsy)
1085
05/24/2010
1086
05/24/2010
CAUSES OF THIRD-SPACING
1087
05/24/2010
ASSESSMENT OF THIRD-SPACING
1088
05/24/2010
PHASES OF THIRD-SPACING
1089
05/24/2010
TREATMENT
1090
05/24/2010
EVALUATION
1091
05/24/2010
1092
05/24/2010
Figure 26.7a
1093
05/24/2010
1094
05/24/2010
1095
05/24/2010
SIGNIFICANT POINTS
1096
05/24/2010
SIGNIFICANT POINTS
1097
05/24/2010
LABS
1098
05/24/2010
INTERVENTIONS
1099
05/24/2010
1100
05/24/2010
Figure 26.7b
1101
05/24/2010
CAUSES
1102
05/24/2010
SIGNS/SYMPTOMS
1103
05/24/2010
SIGNS / SYMPTOMS
1104
05/24/2010
SIGNS / SYMPOTMS
1105
05/24/2010
INTERVENTIONS
1106
05/24/2010
SOURCES OF WATER
1107
05/24/2010
1108
05/24/2010
1109
05/24/2010
1110
05/24/2010
IV FLUID REPLACEMENT
1111
05/24/2010
IV FLUID REPLACEMENT
1112
05/24/2010
ELECTROCHEMICAL EQUIVALENCE
1114
05/24/2010
SOLUTE OVERVIEW:
INTRACELLULAR VS. EXTRACELLULAR
1115
05/24/2010
Protein
Organic Phos.
400 Inorganic Phos
Bicarbonate
300 Chloride
Magnesium
200 Calcium
Potassium
100 Sodium
0 Plasma InterstitialCell
H2O H2O H 2O
1116
05/24/2010
1117
05/24/2010
OSMOTIC PRESSURE ( )
= p
S S S
S
S S S
S S S
S S S
1118
05/24/2010
GLUCOSE EXAMPLE
Initial Gl Gl Gl Gl
10 L 10 L
Final Gl Gl Gl Gl
15 L 5 L
1119
05/24/2010
OSMOTIC CONCENTRATION
in 1L
1mole of CaCl forms a 3 osmolar solution
2
in 1L
Physiological concentrations:
1 mOSM = 10-3 osmoles/L
1120
05/24/2010
1121
05/24/2010
1122
05/24/2010
1123
05/24/2010
PRIMARY DISTURBANCE:
INCREASED ECF OSMOLARITY
1124
05/24/2010
PRIMARY DISTURBANCE:
DECREASED ECF OSMOLARITY
1125
05/24/2010
1126
05/24/2010
1127
05/24/2010
TYPE OF SOLUTIONS
Saline solutions
Come in a variety of concentrations:
hypotonic (eg., 0.2%), isotonic (0.9%), and
hypertonic (eg. 5%).
Dextrose in Saline
Glucose is rapidly metabolized to CO2 +
H2O
The volume therefore is distributed
intracellularly as well as extracellularly
Again available in various concentrations
Used for simultaneous volume replacement
and caloric supplement
Dextran, a long chain polysaccharide
Solutions are confined to the vascular
compartment and preferentially expand
this portion of the ECF
1128
05/24/2010
1130
05/24/2010
1131
05/24/2010
1132
05/24/2010
Factors
affecting ADH
release 1133
05/24/2010
1134
05/24/2010
1135
05/24/2010
•Sodium balance
ü The kidneys - the major site
of control of sodium output
ü Influence of dietary input on
appropriate changes in sodium
excretion by the kidneys
ü Effector mechanisms include
changes in:
-glomerular filtration rate
-plasma aldosterone levels
-peritubular capillary Starling
forces
1136
05/24/2010
1137
05/24/2010
1138
05/24/2010
1139
05/24/2010
Pathway of
RAAS
1140
05/24/2010
1141
05/24/2010
1142
05/24/2010
•Atrial natriuretic
peptide
1143
05/24/2010
1145
Homeostas is : severe
dehydrati on
05/24/2010
1146
05/24/2010
• Potassium balance
ü Potassium plays a number of
important roles in the body
−electrical excitability of cells
−major osmotically active solute in
cells
−acid-base balance
−cell metabolism
ü The kidneys are the major site in
control of potassium balance
1147
05/24/2010
1149
05/24/2010
ELECTROLYTES
Ions
Cations—positive charge
Anions—negative charge
Homeostasis—total cations equal to total
anions
1150
05/24/2010
FLUID BALANCE
• Solvents—liquids that hold a substance in
solution (water)
• Solutes—substances dissolved in a
solution (electrolytes and non-
electrolytes)
1151
05/24/2010
MAJOR ELECTROLYTES/CHIEF
FUNCTION
• Sodium—controls and regulates volume of body
fluids
• Potassium—chief regulator of cellular enzyme
activity and water content
• Calcium—nerve impulse, blood clotting, muscle
contraction, B12 absorption
• Magnesium—metabolism of carbohydrates and
proteins, vital actions involving enzymes
• Chloride—maintains osmotic pressure in blood,
produces hydrochloric acid
• Bicarbonate—body’s primary buffer system
• Phosphate—involved in important chemical reactions
in body, cell division, and hereditary traits
1152
05/24/2010
QUESTION
1153
05/24/2010
ANSWER
Answer: B. False
Molecules in the body’s chemical
compounds that remain intact are called
nonelectrolytes.
1154
05/24/2010
ELECTROLYTES
Ø
Ø salts or minerals in extracellular or
intracellular body fluids
1155
05/24/2010
ELECTROLYTE Composition
Electrolyte Conc Plasma ( mEq / L ) ISF
ICF
Sodium, Na+ 142 141 10
Potassium, K+ 5 4.1 150
Calcium, Ca++ 5 4.1 -
Magnesium, Mg++ 3 3 40
( 155 )
Chloride, Cl- 103 115 15
Bicarbonate, HCO3- 27 29 10
Biphosphate, HPO4- 2 2 100
Sulfate, SO4-2 1 1 20
Protein 16 1 60
Organic foods 6 3.4 -
( 155 )
1156
05/24/2010
ELECTROLYTES
Functions of Electrolytes
1157
05/24/2010
ELECTROLYTES
Hyponatremia [Na+ < 135 mEq/L; Normal = 135-145 mEq/L]
qCauses
ü Na+ intake
ü Na+ excretion [diaphoresis, GI
suctioning]
üAdrenal insufficiency
qAssessment
üN & V, abdominal cramps, weight
loss
üCold, clammy skin, skin turgor
üApprehension, HA, convulsions,
focal neurologic deficit, coma 1158
05/24/2010
ELECTROLYTES
qManagement
üProvide foods high in sodium
üAdminister NSS IV
üAssess blood pressure frequently
[measure lying down, sitting & standing]
1159
05/24/2010
ELECTROLYTES
qCauses
üExcessive, rapid IV adm’n of NSS
üInadequate water intake
üKidney disease
qAssessment
üDry, sticky mucus membranes
üFlushed skin
üRough dry tongue, firm skin turgor
üIntense thirst
üEdema, oliguria to anuria
üRestlessness, irritability [cerebral 1160
05/24/2010
ELECTROLYTES
qNursing Intervention
üWeigh daily
üAssess degree of edema
frequently
üMeasure I & O
üAssess skin frequently & institute
nursing measures to prevent
breakdown
üEncourage sodium-restricted diet
1161
05/24/2010
ELECTROLYTES
qCauses
üRenal insufficiency
üAdrenocortical insufficiency
üCellulose damage [burns]
üInfection
üAcidotic states
üRapid infusion of IV sol’n w/
potassium-conserving diuretics
1162
05/24/2010
ELECTROLYTES
qAssessment
üThready, slow pulse
üShallow breathing
üN & V, diarrhea, intestinal colic
üIrritability
üMuscle weakness, flaccid paralysis
üNumbness, tingling
üDifficulty w/ phonation,
respiration
1163
05/24/2010
ELECTROLYTES
qNursing Interventions
üAdminister kayexalate as ordered
üAdminister/monitor IV infusion of
glucose & insulin
üControl infection
üProvide adequate calories &
carbohydrates
üDiscontinue IV or oral sources of
K+
1164
05/24/2010
ELECTROLYTES
qCauses
üRenal insufficiency
üAdrenocortical insufficiency
üCellulose damage [burns]
üInfection
üAcidotic states
üRapid infusion of IV sol’n w/
potassium-conserving diuretics
1165
05/24/2010
ELECTROLYTES
qAssessment
üThready, rapid, weak pulse
üFaint heart sounds
ü BP
üSkeletal muscle weakness
ü or absent reflexes
üShallow respirations
üMalaise, apathy, lethargy
üLoss of orientation
üAnorexia, vomiting, weight loss
üGaseous intestinal distention
1166
05/24/2010
ELECTROLYTES
qNursing Interventions
üAdminister K+ supplements to
replace losses
üBe cautious in administering
drugs that are not potassium-
sparing
üMonitor acid-base balance
üMonitor pulse, BP and ECG
1167
05/24/2010
ELECTROLYTES
qCauses
üHyperparathyroidism
üImmobility
üIncreased vitamin D intake
üOsteoporosis & osteomalacia
[early stages]
qAssessment
üN & V, anorexia, constipation
üHeadache, confusion
üLethargy, stupor
1168
üDecreased muscle tone
05/24/2010
ELECTROLYTES
qNursing Interventions
üEncourage mobilization
üLimit vitamin D intake
üLimit calcium intake
üNormal saline
üAdminister diuretics
üCalcitonin
1169
05/24/2010
ELECTROLYTES
qCauses
üAcute pancreatitis
üDiarrhea
üHypoparathyroidism
üLack of vitamin D I the diet
üLong-term steroid therapy
qAssessment
üPainful tonic muscle & facial
spasms
üFatigue, dyspnea
1170
üLaryngospasm, convulsions
05/24/2010
ELECTROLYTES
qNursing Interventions
üAdminister oral Ca lactate or
IV CaCl2 or gluconate
üProviding safety by padding
side rails
üAdminister dietary sources of
calcium
üVitamin D
üProvide quiet environment
1171
05/24/2010
ELECTROLYTES
qCauses
üRenal insufficiency, dehydration
üExcessive use of Mg-containing
antacids or laxatives
qAssessment
üLethargy, somnolence, confusion
üN & V
üMuscle weakness, depressed
reflexes
ü pulse and respirations
qNursing Intervention
1172
üWithhold Mg-cont’g drugs/foods;
05/24/2010
ELECTROLYTES
qCauses
üLow intake of Mg in the diet
üProlonged diarrhea
üMassive diuresis
üHypoparathyroidism
qAssessment
üParesthesias, muscle spasm
üConfusion, hallucination, convulsions
üAtaxia, tremors, hyperactive deep
reflexes
üFlushing of the face, diaphoresis
1173
qNursing Intervention
ELECTROLYTE DISORDERS
SUMMARY
SIGNS AND SYMPTOMS
Electrolyte Excess Deficit
Sodium (Na) Hypernatremia Hyponatremia
Thirst CNS deterioration
CNS deterioration
Increased interstitial fluid
05/24/2010 1174
ELECTROLYTE DISORDERS
SIGNS AND SYMPTOMS
Electrolyte Excess Deficit
Calcium (Ca) Hypernatremia Hypocalcemia
Thirst Tetany
CNS deterioration Chvostek’s, Trousseau’s
Increased interstitial fluid Muscle twitching
CNS changes
EKG changes
Magnesium (Mg) Hypermagnesemia Hypomagnesemia
Loss of deep tendon reflexes Hyperactive deep tendon
(DTRs) reflexes
Depression of CNS CNS changes
Depression of neuromuscular EKG changes
function
05/24/2010 1175
05/24/2010
PROTEIN IMBALANCES
1176
05/24/2010
HYPOPROTEINEMIA
1177
05/24/2010
HYPOPROTEINEMIA
HYPOPROTEINEMIA:
CLINICAL MANIFESTATIONS
1179
05/24/2010
HYPOPROTEINEMIA
1180
05/24/2010
1181
05/24/2010
1182
05/24/2010
1183
05/24/2010
1184
05/24/2010
1185
NURSING IMPLEMENTATION FOR
05/24/2010
VOLUME IMBALANCES
Neurologic function
LOC
PERLA
Voluntary movement of extremities
Muscle strength
Reflexes
1186
05/24/2010
IV FLUIDS
1187
05/24/2010
SOLUTION TYPES
1188
05/24/2010
SOLUTION TYPES
1189
05/24/2010
SOLUTION TYPES
1190
05/24/2010
D5W
1191
05/24/2010
D5W
1192
05/24/2010
1193
05/24/2010
1194
05/24/2010
LACTATED RINGER’S
1195
05/24/2010
D5 ½ NS
1196
05/24/2010
D5 ½ NS (HYPERTONIC)
1197
05/24/2010
1198
05/24/2010
Indications
1199
05/24/2010
Types of Solutions
qIsotonic
ü0.9% sodium chloride (NSS)
üLactated Ringer’s sol’n
qHypotonic
ü5% dextrose and water (D5W)
ü0.45% sodium chloride
ü0.33% sodium chloride
qHypertonic
ü3% NaCl
üProtein sol’ns
qColloids
1200
üSalt pour albumin Plasmanate,
05/24/2010
1201
05/24/2010
ELECTROLYTE IMBALANCES
• Hyponatremia and hypernatremia
• Hypokalemia and hyperkalemia
• Hypocalcemia and hypercalcemia
• Hypomagnesemia and hypermagnesemia
• Hypophosphatemia and
hyperphosphatemia
1203
05/24/2010
QUESTION
1204
05/24/2010
ANSWER
Answer: A. Hyponatremia
Rationale:
Hyponatremia refers to a sodium deficit in ECF
caused by a loss of sodium or gain of water.
Hypernatremia refers to a surplus of sodium in ECF.
Hypokalemia refers to a potassium deficit in ECF.
Hyperkalemia refers to an excess of potassium in
ECF.
1205
05/24/2010
BURNS
BURNS
Øwounds caused by excessive exposure to the
following agents or causes:
Causes of Burns:
1206
05/24/2010
BURNS
CLASSIFICATION OF BURNS
BURNS
STAGES OF BURNS
q1st 48 hrs
qIVC ISC
qGeneralized DHN [fluid shifting]
qHypovolemia [plasma loss], BP, C.O.
qHemoconcentration, Hct [liquid blood
component ISC]
qOliguria [ renal perfusion], ADH release
& aldosterone
qHyperK, hypoNa
qMetabolic acidosis
1208
05/24/2010
BURNS
STAGES OF BURNS
qAfter 48 hrs
qISC IVC
qHypervolemia,
qHemodilution, Hct
qDiuresis [ renal perfusion], ADH &
aldosterone secretion
qHypoK, hypoNa [K moves back into the
cells, Na+ still trapped in the edema
fluids
qMetabolic acidosis
1209
05/24/2010
BURNS
STAGES OF BURNS
BURNS
ASSESSMENT
BURNS
ASSESSMENT
9%
Front=18 %
9% Back=18 % 9%
1%
Burn Evaluation
18 % 18 %
Chart
1212
05/24/2010
BURNS
ASSESSMENT
1213
05/24/2010
BURNS
EMERGENCY MANAGEMENT
BURNS
MANAGEMENT
qPreventing infection
qWound care
1215
05/24/2010
BURNS
qSemi-open method
üCovering of wound w/ topical
antimicrobials: 1216
05/24/2010
BURNS
qAllograft
üSkin taken from other person
[cadaver]
ü
qAutograft
üSame person
qHeterograft
üDifferent species
üXenograft [segment of skin from
animal such as pig or dog]
1217
05/24/2010
BURNS
FLUID REPLACEMENT
Types of fluids:
qColloids
üBlood
üPlasma & plasma expanders
qElectrolytes
üLactated Ringers
qNon-electrolyte
üD5W
1218
05/24/2010
BURNS
FLUID REPLACEMENT
EVAN’S Formula:
BURNS
FLUID REPLACEMENT
1221
05/24/2010
secretion
Release of calcium from bone is inhibited
Larger amounts of calcium are lost in feces and
urine
More phosphate is retained
1222
05/24/2010
INFLUENCE OF CALCITONIN
1223
05/24/2010
REGULATION OF ANIONS
1224
05/24/2010
ACID-BASE BALANCE
1225
05/24/2010
1226
05/24/2010
1227
05/24/2010
1228
05/24/2010
1229
05/24/2010
1230
05/24/2010
1231
05/24/2010
1232
05/24/2010
1233
05/24/2010
1234
05/24/2010
1235
05/24/2010
1236
05/24/2010
1237
05/24/2010
1238
05/24/2010
REABSORPTION OF BICARBONATE
1239
05/24/2010
REABSORPTION
• Carbonic acid OF BICARBONATE
formed in
filtrate
dissociates to
release carbon
dioxide and
water
• Carbon dioxide
then diffuses
into tubule
cells, where it
acts to trigger
further
hydrogen ion
1240
Figure 26.12
05/24/2010
1241
05/24/2010
acidosis:
Kidneys
generate
bicarbonate
ions and add
them to the
blood
An equal
amount of
hydrogen ions
are added to
the urine
1243
Figure 26.13
05/24/2010
1244
05/24/2010
AMMONIUM ION
EXCRETION
Figure 26.14
1245
05/24/2010
1246
05/24/2010
Respiratory Metabolic
Acidosis Alkalosis
26 45
HCO3 Normal Ranges PaCO2
22 35
Metabolic Respiratory
Acidosis Alkalosis
7 . 35
pH
7 . 45
1247
05/24/2010
1248
05/24/2010
1249
05/24/2010
METABOLIC ACIDOSIS
1250
05/24/2010
METABOLIC ALKALOSIS
1251
05/24/2010
1252
05/24/2010
RESPIRATORY COMPENSATION
1253
05/24/2010
RESPIRATORY COMPENSATION
1254
05/24/2010
RENAL COMPENSATION
1255
05/24/2010
RENAL COMPENSATION
1256
05/24/2010
DEVELOPMENTAL ASPECTS
1257
05/24/2010
1258
05/24/2010
ACID–BASE IMBALANCES
1259
05/24/2010
NURSING ASSESSMENTS
• Identify patients at risk for imbalances
• Determine a specific imbalance is present
and its severity, etiology, and
characteristics
• Determine effectiveness of plan of care
1260
05/24/2010
PARAMETERS OF ASSESSMENT
• Nursing history and physical assessment
• Fluid intake and output
• Daily weights
• Laboratory studies
1261
05/24/2010
1262
05/24/2010
1263
05/24/2010
1264
05/24/2010
EXPECTED OUTCOMES
• Maintain approximate fluid intake and
output balance (2500 mL intake and
output over 3 days)
• Maintain urine specific gravity within
normal range (1010 to 1025)
• Practice self-care behaviors to promote
balance
1265
05/24/2010
IMPLEMENTING
• Dietary modifications
• Modifications of fluid intake
• Medication administration
• IV therapy
• Blood and blood products replacement
• TPN
1266
05/24/2010
ADMINISTERING MEDICATIONS
• Mineral-electrolyte preparations
• Diuretics
• Intravenous therapy
1267
05/24/2010
INTRAVENOUS THERAPY
• Vascular access devices
• Peripheral venous catheters
• Midline peripheral catheter
• Central venous access devices
• Implanted ports
1268
05/24/2010
QUESTION
1269
05/24/2010
ANSWER
Answer: A. True
Central venous access devices provide
access for a variety of IV fluids,
medications, blood products, and TPN
solutions and allow a means for
hemodynamic monitoring and blood
sampling.
•
1270
05/24/2010
1271
05/24/2010
PLACEMENT OF PERIPHERALLY
INSERTED CENTRAL CATHETER
(PICC)
1272
05/24/2010
1273