Renal Pulmonary pa/ph #1

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Created by:

dourada Plus on September 30, 2011

Subjects:

lccw, renal

Description:

1st half- pulmonary

Classes:

Sherman Class 2015, Boards Part I (NBCE), LCCW quarter 5, LCCW

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Renal Pulmonary pa/ph #1

conducting zone
nose
nasal cavity
pharynx (naso-, oro-, laryngo-)
larynx
trachea
bronchi (23 bifurcations total)
bronchioles
terminal bronchioles
1/140
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Definitions

conducting zone nose
nasal cavity
pharynx (naso-, oro-, laryngo-)
larynx
trachea
bronchi (23 bifurcations total)
bronchioles
terminal bronchioles
respiratory zone respiratory bronchioles
alveolar ducts (stem)
alveolar sacs (bunch of grapes)
alveoli (grapes)
cartilagenous structures
all hyaline
except epiglottis(elastic)
cricoid (C-6)
thyroid
arytenoid
carina (T-4)
hyoid at level of C4
(when x-raying- put horizontal beam through level of hyoid)
cervical x-ray must have all 7 cervicals in x-ray
carina at division of trachea
right primary bronchi shorter, wider, and more vertical
(more likely to aspirate something into the right side-hot dogs, grapes and peanuts)
secondary bronchi aka lobar bronchi
3 on rt
2 on lft
tertiary bronchi segmental bronchi
bronchioles <1mm
no cartilage
terminal bronchiole <0.5mm
alveolar ducts smooth muscle, elastic fibers, and collagen fibers
leads to alveolar sacs
alveoli ~300 million in lungs
-simple squamous=type I (gas exchange)
-cuboidal=type II (secrete surfactant-decrease surface tension)
-surrounded by elastic fibers
alveoli and capillaries fused with basal lamina
form respiratory membrane
alveolar pores connect adjacent alveoli
equalization of air pressure
detour for air routes
alveolar macrophages aka dust cells
swallow approx 2 million dead mac's per hour
phases of respiration inspiration
expiration
atmospheric pressure produced by air surrounding the body
760mmHg, 14.7 psi at sea level
Intrapulmonary pressure pressure w/in alveoli/lungs
rises and falls with phases of breathing
(higher than intrapleural)
intrapleural pressure pressure w/in pleural cavity
~4mmHg less than intrapulmonary pressure
elastic recoil attempts to pull lungs away from inside of thoracic wall
lung recoil caused by elasticity of lungs
-always try to assume smallest size possible
-and surface tension of alveolar fluid that constantly acts to draw the alveoli to their smallest dimension
elastic property of thoracic wall -opposes elastic property of lungs
-tends to pull outward this creating enlargement of lungs
surface tension b/t lungs and thoracic wall creates negative 4mmHg intrapleural pressure
lung collapse
-thorax
(accumulations in pleural cavity)
equalizes the intrapleural and intrapolmonary pressure
-common in chest wounds
pneumo- (air)
hemo- (blood)
pyo- (pus-purulent exudate)
pneumothorax abnormal presence of air in the pleural cavity resulting in the collapse of the lung
hemothorax accumulation of blood in the pleural cavity (the space between the lungs and the walls of the chest)
pyothorax presence of pus in the pleural cavity between the layers of the pleural membrane
Boyle's Law P1V1=P2V2
(if temp is constant)
the volume of the gas increases as the pressure of the gas decreases
and the volume of the gas decreases as the pressure of the gas increases
greatest resistance to flow occurs in medium sized bronchi
direct result of drag or friction w/in passageways
surfactant 80% phospholipids
10% neutral lipids
10% protein
forced inspiration occurs with physical exertion or w disease process
creates overall increase in volume of thoracic wall
inspiration lowering of diaphragm creates increase in superior to inferior increase in container->air rushes into container
expiration rise in intrapulmonary pressure ~1mmHg above atomospheric- forces air out
-created by natural elasticity of lungs
forced expiration active process
recruitment of thoracic and abdominal muscles
tidal volume (TV) the amount of air inhaled or exhaled under normal resting conditions
~500ml
inspiratory reserve volume (IRV) amount of air forcefully inhaled after a normal TV inhalation
~3100ml
expiratory reserve volume (ERV) amount of air forcefully exhaled after a normal TV exhalation
~1200ml
residual volume (RV) amount of air remaining in lungs following a TV and ERV exhalation
~1200ml
total lung capacity (TLC) TV+IRV+ERV+RV
~6000ml
alveolar surface tension produced when liquid molecules are strongly attracted to each other
alveolar film water and surfactant
(water highly polar-too much surface tension-would cause collapse)
surfactant-produced by Type II cells
IRDS too little surfactant production-causes collapse of lungs
vital capacity amt of air that can be inhaled/exhaled TV, forced inhalation, focred exhalation
TV+IRV+ERV
should be ~80% of TLC
~4800ml
inspiratory capacity amount of air that can be inhaled following a normal T.V. exhalation (TV+IRV)
~3600ml
functional residual capacity (FRC) volume of air remaining in lungs after TV exhalation
ERV+RV
~2400ml
anatomical dead space ~350ml reach alveoli
~150 in conducting zone,
Includes air in the conducting respiratory passages, air not used in gas exhange
alveolar dead space pathology emphysea
->loss of elastic tissue in lungs
-can get air in- can't get air out
(pink puffers and blue bloaters)
total dead space alveolar +anatomical
anemic hypoxia decrease RBC's - decrease hemoglobin
decrease ability to deliver oxygen
ischemic/stagnant hypoxia blockage or impairment to circulation
to lungs: pulmonary embolism- often misdiagnosed as heart attack (golden hour-anti-coagulant)-symptoms severe chest pain, shortness of breath
(left sided CHF-full body ischemia)
histotoxic hypoxia cellular poisoning (cyanide/arsenic)
decrease cellular oxygen uptake
hypoxic hypoxia reduced arterial oxygen
i.e. emphysema, COPD, carbon monoxide (200x greater affinity than oxygen-nausea, headache, vomiting, loss of consciousness, cherry red)
Dalton's law of partial pressure total pressure exerted by a gas mixture is equivalent to the sum of the gases found in the mixture
partial pressure the pressure exerted by a single gas (in a mixture)
directly proportional to its percentage of the total gas mixture
atmospheric air nitrogen 78.6%
oxygen 20.9%
CO2 0.04%
H2O 0.46% (water vapor)
non "primary" respiratory air movement -talking
-coughing
-singing
-sneezing
-hiccup
-yawning
-laughing
-cry
external respiration exchange in lungs
internal respiration exchange in cells and tissues of body
amt of blood 5-6L
temp of blood 100.4 F
blood pH 7.45-7.45
PPO2 in lungs 40mmHg in Pulm A to 104mmHg in Pulm V
PPCO2 in lungs 45mmHg in Pulm A to 40mmHg in Pulm V
solubility of gases CO2 ~20x more soluble than O2 in blood
CO2 transport in blood bicarbonate (60-70%)
bound to RBC (20-30%)
dissolved in plasma (7-10%)
Hemoglobin 4 polypeptide chains bound to iron-containing heme group
capable of binding 4 O2 molecules (=oxyhemoglobin HbO2)
iron is oxygen binding
Hb with no O2 deoxyhemoglobin or reduced hemoglobin
reverse binding is due to pH, PO2, PCO2, temp, and BPG
air composition comparison atmos-mainly N2 and O2
alveolar-more CO2 and water vapor (less O2)
-newly inspire air of tidal volume mixed with remaining gases w/in respiratory passages
humidification of air in conducting passages
gas exchange equilibrium time less than 0.25 sec
hypercapnia high CO2
acidic condition (blood, CSF)
slow respiration-emphysema, alcohol/drugs, head trauma
hypocapnia too little CO2
-hyperventilation-faint, dizziness- use brown bag
hyper/hypo-ventilation over/under breathing
Apnea cessation of breathing
anatomical:
pharyngeal
respiratory center
Dyspnea difficulty breathing
asthma emphysema, pneumonia
tracheal-esophageal anomalies tracheal-esophageal fistula
most common anomaly of larynx and trachea
-swallowed food can be aspirated into bronchi
epiglottis infection caused by haemophilus influenzae type B
-air flow obstruction
-most common in infants and young children
-inspiratory stridor
croup stridor, cough, and hoarseness
-epiglottitis and laryngotracheobronchititis
laryngitis inflammation of larynx causes hoarseness, normally viral
tracheitis inflammation of the trachea causes coughing
normally viral
laryngeal carcinoma most are squamous cell carcinoma
directly related to smoking
whooping cough caused by Haemophilus pertussis
S&S: fever, severe bouts of coughing and a whooping sound on inspiration
most common cause of cancer death in US lung cancer (rare until 1945-now epidemic)
squamous cell carcinoma normally slow growing
found in major bronchi due to smoking
adenocarinoma -most common primary malignant lung tumor
-glandular appearance of lung
-commonly found in lung periphery
-assoc mucus secretion
-faster growing than squam-cell carcinoma
-may invade pleura
small/Oat Cell carcinoma form in apex -Pancoast tumor
-brachial plexus above cupola (P/T/N)
-Horner's Syndrome(ptosis, meiosis, anhydrosis- loss of sympathetic to head and neck)
-x-ray-> apical lordotic
-highly malignant
-sheets of small tumor cells
-aka oat cell also intermediate cell carcinoma
-early metastasis- makes them inoperable
metastatic tumors most common malignant tumors of lungs
typically appear multiple and well defined
strep Pn middle aged adults
alcohol abuse
fever, chills, thoracic pain, pleuritis, rust colored hemoptysis, massive amts of PMN's
kb pn alcoholism
lobar pneumonia
tissue necrosis
abcess formation
bronchopleural fistula
staph pn following influenza
many small lung abcesses
infants-pneumaoceles"
tension pneumothorax
gram negative pneumonia -E.coli: pneumonia due mainly to GI surgery complication
-or pseudmonas aeurigenosa: mostly seen in immunocompromised individuals, burn pts and cystic fibrosis
Legionell's Disease * -legionella pneumophilia
-named due to 1976 outbreak in Philly, PA American Legion convention
-occurs in hotels, hospitals, nursing homes due to contaminated air circulation
-S&S: fever, muscle ache, malaise and abdominal pain
-most victims are immunocompromised
-may result in alveolar pneumonia
Tuberculosis mycobacterium tuberculosis
-hardy bacteria
-persist for long period of time
-droplet inhalation-most common infective pathway
-initial infection-> macrophage infiltration, caseous necrosis and granulmatous lesions
-bacteria can still replicate even if ingested by macrophages
pulmonary edema increase hydrostatic pressure
decrease oncotic pressure
obstruction of lymphatic system
hydrostatic pressure force exerted by fluid in equilibrium due to the force of gravity (force exerted by fluid against capillary wall)
increase causes: L sided heart failure and mitral stenosis
oncotic pressure to maintain fluid w.in capillaries
decrease causes: malnutrition, proteinuria, hypoalbuminemia,
[The osmotic pressure in the blood vessels due only to plasma proteins (primarily albumin) --> causes water to rush back into capillaries at end.]
Edema due to microvascular injury -infection in lungs -> inflammatory response
-inhalation of substances- smoke, fluid, foreign particles, chemicals-tissue damage (i.e. O2 at too high concentrations is toxic and irritates tissues)
-ingested substances
-sepsis, shock, trauma, heat, embolism, radiation
edema treatment diurectics
diffuse alveolar damage S&S cyanosis, tachycardia, and respiratory insufficiency
-result of diffuse capillary damage
-collapsed leathery looking lung- difficult to inflate
causes of diffuse alveolar damage viral, radiation, poison gases, overdoses of narcotics, oxygen
diffuse alveolar damage (DAD) microscopically alveoli lining loss
fluid exudation
formation of hyaline membranes
-fibrin, fluid filled protein, necrotic epithelial cells
DAD: hyaline membranes usually occur in Infant Respiratory Distress Syndrome
-caused by deficiency of pulmonary surfactant
pulmonary infarct direct result of pulmonary embolism
-leads to decrease or loss in circulation
pulmonary infarct lower lobes 75%
-most cases hemorrhagic
-may extend to pleura producing fibrous exudates
obstructive pulmonary disease increase in resistance to air flow w/in respiratory passages
-asthma, pneumonia, COPDs, bronchitis
restrictive pulmonary disease decrease in total lung capacity
-DJD, DISH, scoliosis, ankylosing spondylitis, subluxation, rib fractures, pleuritis, pectus excavatum pectus carniatus
diffuse lung fibrosis: causes -incomplete resolution of viral and bacterial infection
-industrial lung disease
industrial lung diseases asbestosis-mesothelioma
coal miners lung-anthracosis
cotton dust-byssinosis
valley fever-histoplasmosis
carcinoma cor pulmonale
R ventricular hypertrophy due to vasoconstriction
bronchiectasis -copious quantity of purulent sputum
-infection of bronchi and bronchioles resulting in abnormal dilation
bronchiectasis: causes bronchial obstruction
hereditary- cystic fibrosis
pneumonia
bronchial obstruction tumor-squamous cell
aspiration of substance causing inflammation
hereditary cystic fibrosis (recessive)
excess mucus in lungs and pancreas
dx-sweat test
treatments- salty air, postural drainage, vibration
chronic bronchitis -at least 3 months of sputum production for 2 or more yrs
-hypertrophy of mucus glands
-squamous cell metaplasia
nosocomial most common pneumonia in hospitals from staph
80-90,000 deaths per year
asthma characterized by spastic contraction of the smooth muscle of the bronchioles
extrinsic asthma -allergic reaction IgE mediated mainly attached to mast cells in lungs
-foreign object inhaled-reaction w mast cell attached antibody
-resulting dyspnea from reaction and contraction of smooth m w decreased expiratory rate
asthma viral infections causing increase in symptoms
most common in children <2yoa
ASA (aspirin) sensitivity: asthma -recurrent rhinitis
-nasal polyps
-inhibits cyclo-oxygenase-1 enzyme [-which helps in formation of prostaglandins]
prostagladins -regulate inflammatory response
[Substances resulting from interactions involving arachidonic acid and acting as mediators in type I hypersensitivity reactions.]
asthma pathology -mucus
-thickening of BM
-hypertrophy of smooth m in bronchi and bronchioles
-Charcot-Leyden crystals (eosinophil membrane proteins)
-increased residual volume and functional residual capacity
-barrel chest occurs over time due to changes in breathing habits
intrinsic asthma viral infection
Emphysema destruction of alveoli
50% of all autopsies show emphysema
destruction of elastic tissue in lungs
-destruction of alveolar walls with enlargement of air spaces distal to respiratory bronchioles
panacinar alveoli appear enlarged
individual is able to get air into lungs
cannot properly exhale
-alveoli involvement
centriacinar Type of emphysema caused by smoking
-Involves alveoli and Respiratory Bronchioles
smoking causes deficiency of alpha-1-antitrypsin
elastic tissue is replaced by fibrotic "scar tissue"
alpha-1-antitrypsin produced in the liver
protects against elastase enzyem which breaks down elastic tissue
smoking #1 cause of emphysema
emphysema complications death
hypoxia
ventricular hypertrophy (R-mainly or first but could be both)
polycythemia- increased RBCs
pneumoconiosis disease process due to inhaled inorganic substances
-asbestos
-silicosis- silica sand- glass, sand blasting
rhinitis inflammation of the nasal cavity
sinusitis inflammation of the sinuses
laryngitis inflammation of the larynx
tracheitis inflammation of the trachea
epiglotitis inflammation of the epiglottis
pleuritis inflammation of the pleura
bronchitis inflammation of the bronchi
pneumonitis inflammation of the alveoli

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