Upgrade to remove ads
Pathophys, Exam 3: Pulmonary/Respiratory
Terms in this set (84)
In terms of gas exchange, what is the terminal portion of the lungs?
What are alveoli very close to and why?
-very close to pulmonary capillaries
-allows good gas exchange/mixture of oxy and deoxy blood
What system plays a role in removing particles from interstitial spaces of the lung?
What are the pores of Kohn?
-alveoli are not a closed system
-these pores allow for air mixing
What are the differences between Type I and Type II alveolar cells?
-Type 1: 95% of alveoli surface; don't divide; form barrier between air inside and wall component
-Type II: 5% of alveoli surface; dividing cells - progenerate Type I and Type II; make pulmonary surfactant
What is the function of pulmonary surfactant? What produces it?
-helps keep lungs compliant; allows lungs to inflate fully
-produced by Type II alveolar cells
What is the function of alveolar macrophages?
-remove offending substances
What do the diaphragm and intercostal muscles do during inspiration?
-diaphragm: contracts and moves downward when you inspire
-intercostal muscles: contract during inspiration to allow expansion and to allow the sternum to move forward for proper inflation
What kind of process is expiration? What does the diaphragm do?
-diaphragm recoils to original position
Someone who has trouble breathing will start using extra muscles to breath, what are these muscles?
-accessory muscles: trapezius, scalenus, sternomastoid
What is dyspnea? What 4 mechanisms can cause it?
-subjective feeling of difficulty breathing
-mechanism: stimulation of lung receptors
-mechanism: increased sensitivity to changes in ventilations perceived through CNS mechanisms
-mechanism: reduced ventilatory capacity or breathing reserve
-mechanism: stimulation of neural receptors in the muscle fibers of the intercostals and diaphragm
Explain how stimulation of lung receptors can cause dyspnea. (hint: 3 diff receptor types)
-there are a few different types of receptors in the lungs
-stretch receptors sense bronchoconstriction and can lead to the feeling of SOB
-irritant receptors are triggered by cold air, cig smoke, etc.
-J receptors sense lung congestion (such as in pneumonia), cause feeling of SOB
Explain how increased sensitivity to changes in ventilations perceived through CNS mechanisms can cause dyspnea.
-we have 2 different centers in the brain (specifically the medulla)
-they are CNS centers that send out impulses for breathing -- a change here could trigger SOB
Explain how reduced ventilatory capacity or breathing reserve can cause dyspnea.
-this is primarily in COPD pts
-everyone has a breathing reserve when they are not active/not using lungs fully
-COPD pts have obstructive processes and alveoli are destroyed --> they lose their breathing reserve so they never feel like they take a really full breath
Explain how stimulation of neural receptors in muscle fibers of the intercostals and diaphragm can cause dyspnea.
-our body has neural receptors constantly sensing if we have low O2 or high CO2
-their response to either of these conditions is to hyperventilate --> produces SOB feeling + muscles working harder to breathe
What does forced vital capacity (FVC) measure?
maximum amount of air that can be rapidly and forcefully exhaled from the lungs after full inspiration
What does forced expiratory volume (FEV1) measure?
volume of air expired in the first second of FVC
What does FEV1/FVC ratio measure?
volume of air expired in the first second, expressed as a percentage of the FVC
According to the National Heart, Lung, and Blood Institute, what three different things must be occurring in asthma?
-airflow obstruction (relates to bronchoconstriction)
Are asthma symptoms reversible or irreversible?
reversible (someone w/an acute episode can be given tx to make bronchoconstriction go away)
In Missouri, asthma mortality rates are higher in what race?
What are type 1 hypersensitivity reactions?
-MUST be exposed to an allergen
What is IgE? What does it do? (in hypersensitivity rxn)
-principal antibody mediator
-when exposed to a trigger, B cells produce IgE secreting plasma cells
-multiple exposures = IgE detected in blood
What do T-helper (T-lymphocyte) cells do? (in hypersensitivity rxn)
-memory -- remember previous exposure = faster rxn second time around
What are mast cells? What do they do? (in hypersensitivity rxn)
-principal effector cells (driver cell in cascade initiation)
-filled with vesicles filled with cytokines -- proinflammatory mediators
-allergen exposure = binds IgE and degranulation occurs -- cytokines/mediators released from vesicles
What is histamine? What does it do? (in hypersensitivity rxn)
-most important mediator
-H1 receptor is primary driver of hypersensitivity rxn -- may add heartburn med to Benadryl to get H2 receptor too though
-causes smooth muscle contraction and vasodilation (leaky vessels; edema) -- induces bronchoconstriction
-increases mucosal edema
What do eosinophils do? (in hypersensitivity rxn)
primary cell responsible for inflammation
What do alveolar macrophages do? (in hypersensitivity rxn)
-scavengers found in large and small airways
-initiate inflammatory cascade
What do neutrophils do? (in hypersensitivity rxn)
-not as predominate as eosinophils
Histamine, prostaglandins, thromboxanes, leukotrienes, and platelet-activating factor are all what? What are they released from? What do they contribute to?
-are all hypersensitivity rxn mediators
-released from mast cells
-all contribute to bronchospasm
What is an atopic pt?
someone characterized as hyperallergic
What is extrinsic (atopic) asthma?
-induced by exposure to an allergen
-develops within 10-20 minutes of exposure
-characterized by an early and late phase rxn
What are potential triggers for extrinsic (atopic) asthma?
-sulfite containing foods (dried fruit, beer, wine, shrimp)
-seasonal outdoor allergens
What are the 5 "steps" in the early-phase of extrinsic (atopic) asthma?
1. fast onset: within minutes of allergen exposure
2. trigger = antigen (allergen)
3. release of cytokines: antigen binds IgE coated on mast cell, initiating response; epithelial cells of the airway open up and let mast cells and allergens into the airway; degranulation of mast cells occurs = cytokines/mediators released
4. increase in mucus/edema: goblet cells increase mucus production; histamine makes vessels leaky = edema
5. bronchospasm: mediators can directly induce bronchospasm; mediators also attract inflammatory cells (part of late-phase)
What are the 4 "steps" of late-phase extrinsic (atopic) asthma?
1. recruited cells drive the response: can occur 4-8 hrs after early phase; eosinophils and neutrophils were brought to the area by cytokine mediators
2. airway epithelial cells also release eotaxin: eotaxin is an activator of eosinophils -- another way of continuing inflammatory cascade
3. epithelial cell injury occurs as a result of this process and further bronchoconstriction occurs: mucus build-up reduces airflow; edema occurs because of histamine and leaky vessels
4. increased airway responsiveness = prolonged asthma symptoms
What makes extrinsic (atopic) asthma so dangerous? (hint: late phase)
-late phase can occur 4-8 hrs after early phase
-late phase can have worse symptoms = dangerous
What is intrinsic asthma? What are potential triggers?
-triggers: respiratory tract infections; exercise; stress; laughter; cold air; GERD; medications (aspirin, NSAIDs, beta blockers)
What is the asthma triad?
-dx of asthma, true aspirin allergy, nasal polyps
How do NSAIDs and aspirin relate to the asthma response?
-aspirin and NSAIDs decrease prostaglandins but the other side of the pathway is leukotriene production, so we make more of these
-leukotrienes are a common mediator of the asthma response
What are special considerations for using beta-blockers in asthma and COPD pts?
-there are specific and non-specific beta-blockers
-non-specific beta blockers work on beta-2, primarily in the lungs = DO NOT use in asthma patients --> would cause bronchoconstriction; would be okay to use in COPD pts
What is the clinical presentation of asthma? What is the primary symptom?
-wheezing - primary symptom
-dyspnea and chest tightness
-tachypnea and tachycardia
What is wheezing?
-primary symptom of asthma
-high pitched whistling
-usually heard on expiration but can be heard on inspiration too if bad enough; wheezing can disappear entirely if asthma is very bad
Why do tachypnea and tachycardia occur in asthma?
-cardiac and respiratory system are working much harder to move air
-trying to compensate by breathing faster and working the heart harder
What system can asthma patients use on their own to determine how much "trouble" they are in?
-use peak flow meters in the peak flow zone system
-green, yellow, and red zones
-calculated off personal best peak flow
What 5 components do we look at to determine the stage of asthma?
-frequency of symptoms
-beta-agonist use (albuterol)
-interference with activity
-lung function (FEV1 and FEV1/FVC)
What are the two general classes of asthma meds?
-rescue medications (short-acting beta agonists and oral corticosteroids)
-controller medications (mainstay of therapy is inhaled corticosteroids) -- pt takes these all the time
What is an asthma exacerbation? What is a moderate vs severe exacerbation?
-event characterized by a change from the pt's previous status
-moderate: troublesome to patient and prompt a need for change in tx
-severe: require urgent action from MD to prevent hospitalization or death
What are risk factors for asthma-related death?
-history of severe exacerbations
-greater than or equal to 2 hospitalizations for asthma in the past year
-greater than or equal to 3 emergency dept visits for asthma in the past year
-using more than 2 canisters per month of short-acting beta agonist (SABA)
-current oral steroid use
-low socioeconomic status (risk factors b/c of access to tx; often use emergency dept)
What 8 symptoms/signs do we consider when evaluating an asthma exacerbation?
-breathlessness (when does it occur? at some point they can't get a good breath laying down)
-talks in (sentences, phrases, words, can't speak)
-alertness (agitation; lethargy = v. bad)
-accessory muscle use
What is COPD?
-presence of airflow limitation
-associated with enhanced, chronic inflammatory response in the airways and the lungs to noxious particles and gases
-exacerbations and comorbidities contribute to overall severity in individual patients
What two terms are essentially types of COPD but are no longer used and have NO clinical relevance? (i.e., COPD is basically an umbrella term now)
-chronic bronchitis: chronic productive cough for 3 months in each of two successive years in a pt in whom other causes of chronic cough have been excluded
-emphysema: abnormal permanent enlargement of the airspaces distal to the terminal bronchioles accompanied by destruction of their walls and without obvious fibrosis
Is COPD reversible or irreversible?
IRREVERSIBLE (progressive, chronic inflammation and airflow limitations)
The majority of COPD deaths are caused by what?
Compare asthma and COPD. Consider onset, reversibility, symptoms, what drives response, and if genetics plays a role.
-onset early in life
-atopy and eosinophilia drive response
-family history of asthma
-onset later in life
-not fully reversible
-symptoms progressively worsen
What are risk factors for COPD and which one is major?
-smoke, second-hand smoke (>90% of cases - major!)
-occupational exposure (industrial pollutants; pesticides)
-indoor air pollution (more in third world countries)
-low birth weight/history of respiratory infections
-heredity (alpha-1-antitrypsin deficiency; very rare)
True or false: the risk factors for COPD are associations that have been established, NOT cause and effect relationships
What is the function of collagen?
-provides lung structure
-prevents airway collapse
What is the function of elastin?
-helps lungs stay compliant
-helps lungs stretch for full expansion when you take a breath
What is the function of proteases and antiproteases in the lungs?
-proteases digest proteins -- in particular, elastase
-antiproteases protect against protease activity -- loss of antiprotease activity = loss of protective effect in lungs
What are the inflammatory mediators in COPD?
-chemotactic factors: attract neutrophils to airway --> leukotriene B4 (LTB4), interleukin-8 (IL-8)
-proinflammatory cytokines: cause chronic inflammation --> tumor necrosis factor alpha (TNF-alpha), interleukin-6 (IL-6)
-growth factors: can cause fibrosis/hardening of small airways --> transforming growth factor-beta (TGF-beta)
How do triggers (esp smoking) cause the emphysema component of COPD?
-cig smoke attracts inflammatory cells and chemotactic factors to the airway
-neutrophils release elastase (a protease that digests elastin, which helps keep lungs stretchable and compliant) -- normally, we try to inhibit elastin action by alpha1-antitrypsin but smoking/irritants decrease alpha1-antritrypsin activity = take away protective effect
-overall, destruction of elastic fibers in lung occurs; over time this leads to loss of ability to move air out, hard time exhaling air -- it gets trapped; and can collapse bronchioles and cause alveoli dysfunction
-once the damage is done, you can't undo it
Explain the chronic bronchitis component of COPD.
-exposure to irritants (such as cig smoke) occurs
-increased bronchial wall thickness potentiates airflow obstruction
-large airways have enlarged submucosal glands which oversecrete mucus
-small airways experience an increase in goblet cells = mucus plugging of airway lumen and inflammation = air can't get out
-overtime, dysfunction/decrease in cilia = cilia lose their function = more prone to viral, bacterial resp infections
Explain air trapping in COPD pts.
-air trapping occurs -- inflammation decreases air in and hyperinflation decreases air out -- hyperinflation occurs because of decreased elastic stretch (don't move in and out, lost elastic recoil)
Explain the effects on gas exchange in COPD pts.
-destruction of alveoli = hypoxemia --> low blood oxygen levels because not moving air well
-pulmonary vasoconstriction occurs because the vascular system is trying to trickle blood supply in for better gas exchange --> but you aren't blowing off CO2 = hypercapnia (increased CO2)
Explain the ventilation (V) and perfusion (Q) mismatch in COPD.
both of the following can happen in different areas of the lung in diff COPD pts
low V/Q ratio:
-areas of low ventilation
-air has low oxygen levels
-near normal perfusion
-air exchange is bad, blood is okay
-get vasoconstriction because body is saying don't send blood here because ventilation supply is not good = hypoxic vasoconstriction
high V/Q ratio:
-near normal ventilation
-large "dead" air spaces
-areas of no/low perfusion
-good airflow but no perfusion to do anything with it so send it to another area, lung tries to compensate = bronchoconstriction
What is clinical presentation of COPD?
-sputum production (more than asthma pts)
-respiratory failure (in severe cases)
-barrel chest (unique to COPD; lungs hyperinflated)
-use of accessory muscles
What is the difference between blue bloaters and pink puffers in COPD?
either will have prolonged expiration (any COPD pt has this)
-right sided heart failure
-use of accessory muscles
-pursed-lip breathing (trying to breathe through straw)
How is FEV1 and FEV1/FVC ratio in pulmonary function tests?
-decreased FEV1 overall
-lower ratio (decreased FVC too)
Would COPD improve w/albuterol? With time?
The FEV1/FVC ratio must be less than what for dx? (part of GOLD classification of severity of airflow limitation)
less than 70%
What three things do we look at to classify COPD severity?
-FEV1/FVC ratio (GOLD classification)
What is the ONLY therapy that slows COPD progression?
What are non-pharm strategies for smoking cessation?
-taper each day
-brief counseling at each visit
-change your routine
-surround yourself with great support system
What is a COPD exacerbation?
worsening of respiratory symptoms that is beyond day-to-day variations and requires a change in medication to treat
What are the three COPD exacerbation etiologies?
-air pollution (indoor or outdoor)
-unknown 30% of the time
What are the 5 consequences of COPD exacerbations?
-negative impact on quality of life
-impact on symptoms and lung function
-increased economic costs
-accelerated lung function decline
overall: pt never makes it back to where they were (progressive decline)
What are the 3 cardinal symptoms of COPD exacerbations?
-increased sputum purulence (change in sputum color)
-increased sputum volume
What is COPD exacerbation staging?
-1 symptom = mild
-2 symptoms = moderate
-all 3 symptoms = severe
What leads to cor pulmonale in COPD?
-pulmonary hypertension: because of destroyed alveoli, lost alveolar capillaries, and thickening of smooth muscle in pulmonary vessels
-persistent hypoxemia: vasoconstriction of pulmonary vessels; shunt blood to areas that are well ventilated
-ultimately --> cor pulmonale
What is cor pulmonale?
-complication of COPD
-right-sided heart failure from lung disease
-increased resistance in pulm artery means the blood backs up in right side of heart
-clinical manifestation: RV hypertrophy, peripheral edema, SOB, decreased exercise tolerance
What is polycythemia vera?
-not as common as cor pulmonale
-kidneys sense chronic hypoxemia = increased erythropoietin production
-leads to more RBCs produced
-consequences: increased risk for blood clots; tx with periodic phlebotomy, oxygen therapy
What are the 3 major complications of COPD?
-acute respiratory failure
What is acute respiratory failure as a COPD complication?
-gets back to V/Q mismatching and poor gas exchange
-retention of CO2 (hypercapnia)
-decreased oxygen (hypoxemia)
-confusion, somnolence, coma
What is oxygen therapy and when is it indicated?
-not for everyone with COPD
-indicated in pts with O2 saturation < 88% and polycythemia vera, pulmonary HTN, signs of right-sided heart failure
-must be used at least 15 hrs/day or morality benefit
-goal O2 sat: >90-92% --> do NOT try to push 97-100% because low O2 levels are driving respiration, could lose this driver if it is suddenly fixed
THIS SET IS OFTEN IN FOLDERS WITH...
Pathophys, Exam 3: Multiple Sclerosis
Pathophys, Exam 3: Seizure Disorders
Pathophys, Exam 1: Altered Health in Children (8.2…
Pathophys, Exam 3: Schizophrenia & Bipolar Affecti…
YOU MIGHT ALSO LIKE...
Obstructive Pulmonary Disorders
Asthma and COPD Pathophysiology
Pathophysiology CH. 20: Asthma and COPD
Pathophysiology - Respiratory/Pulmonary…
OTHER SETS BY THIS CREATOR
Federal and MO MPJE 2017
Brand/Generic NAPLEX 2019