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28 Cards in this Set
- Front
- Back
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State the etiologies of emphysema
(5) |
1- age- degenerative process
2- alpha 1 antitrypsin deficiency 3- chronic irritation 4- secondary to chronic bronchitis, asthma or other lung condition. 5- altered chest condition |
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Define the two pathological of emphysema
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1 - centralobular - lesions occur around the small bronchioles in the upper airways
2 - panulobular - clusters of big air sacs or lesions involve the periphery of the acinus, middle lobe and lower lobe. |
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What agents are responsible for tissue breakdown?
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alveoli fuses, less surface area, forms the following:
Cyst- small Bleb- moderate Bolus- large causes air trapping |
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List the clinical features found in emphysema
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look at Pink Puffer for symptoms
use of accessory muscles- tripod position distended neck veins barrel chest dypsnea or SOB tachypnea with prolonged exhalation Also: decreased blood return decreased blood pressure decreased cardiac output cor pulmonale |
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List the lab results found in emphysema
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chest xray- barrel chest, flattened diaphragm,
PFT- because of air trapping = increased RV, FRC and TLC FVC and FEV1 decreased because of airflow obstruction ABG resp alkalosis with moderate hypoxemia in mild to moderate emphysema and resp acidosis with more severe hypoxemia generally occurs during acute exacerbations and the terminal stages of the disease. |
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Pink Puffer vs Blue Bloater
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Pink Puffer: dypsneic cachetic (SOB and underweight). leans toward emphysema, large or hyperexpanded lungs, less secretions, pursed lips, retraction or depressed notches in the clavicular or sternal notch, distended neck veins, use of accessory muscles, older patients, ABG: slightly lower PCO2 with a normal PO2
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Blue Bloater vs Pink Puffer
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Blue Bloater: cardiac polycythemic, leans toward, chronic bronchitis, overweight, cardiac issues: cardiomegaly, CHF, increased secretions, increased cough, ABG would show an increased CO2 with hypoxia and a decreased PaO2, more hb or blood cells, younger patients, no tripoding or notch depressed
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cardiac polycythemic is what?
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an increase in red cell mass caused by increased erythropoiesis, which may occur as a compensatory physiologic response to tissue hypoxia
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What are two other types of emphysema
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compensatory - lungs fill and overexpand to fill voids. lungs hyperexpand to fill chest cavity.
subcutaneous- leakage of air outside of lung into chest wall, face, shoulder, neck chest |
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Define emphysema
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an anatomical alteration of the lung characterized by abnormal enlargement of the air spaces accompanied by destructive changes to the alveolar and airway walls.
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what are the different types of alpha 1 antitrypsin deficiency?
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m variant: normal - 250 mg/100 ml
s variant: intermediate - less than 50 mg/100 ml z variant- true disease- less than 50 mg/ 100 ml |
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what is the treatment for alpha 1 deficiency?
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tx- prolastin - plasma derived, given by IV every week or gene therapy
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what is the pathophysiology of emphysema?
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destruction of lung alveolar tissue. tears in the alveolar septa, loss of surface area and less recoil in lung tissue with an increase in lung size. Also damage to capillary bed will cause V/Q mismatch due to loss of surface area.
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chest xray for emphysema will look like what?
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flattened diaphragm
hyperexpanded lungs barrel chest increased AP diameter narrow heart |
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chest xray for COPD chronic bronchitis Blue Bloater will look like what?
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enlarged heart
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What will breath sounds sound like in a chronic bronchitis or blue bloater patient?
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increased secretions
crackles |
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what will breath sounds sound like in an emphysema patient
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diminshed without adventitious (normal) breath sounds
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PFT will be what in COPD?
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decreased flow
FEV below predicted due to air trapping, FVC, - normal to slightly increased RV, TLC and FRC increased due ot air trapping severe V/Q mismatch |
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Treatment for COPD
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smoking cessation
ventilation oxygen hydration meds bronchial hygiene rehab family support education excercise decreased allergens surgical or laser resections or lobectomy |
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Complications for COPD
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pneumothorax, bronchial infections, cor pulmonale (emphysema), pulmonary emboli, acute respiratory failure, chronic hypoxia which affects brain, kidneys liver, stomach
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Describe the pathophysiology of extrinsic asthma
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1- allergen exposure
2- water soluble proteins- broken down and absorbed by lymph tissue 3- IgE antibody formation in response to water soluble proteins 4- mast cell and basophil sensitization. Actual reaction: inflammation, swelling, bronchoconstriction. |
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Describe the pathophysiology of challenge reaction (all types of asthma)
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1- re-exposure or internal response
2-degranulation -true mast cell degranulation 3- physiologic response: massive bronchospasm and broncho constriction, increased BP, hypersecretions, inflamatory response: edema, increased esinophil infiltration substances released: histamines, leukotrienes, SRS-A, bradykinins, seratonin, prostaglandins |
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State the clinical features of all types of asthma
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anxiety
cough - congested and rattling increased white mucus breath sounds- wheezing (broncho-constriction) severe- diminished ABG- early on: alkalotic, hypocapnia plus hypoxia because of hyperventilation decreased CO2, decreased PaO2 later on: flip flop because patient is tired. acidotic, hypercapnea, increased CO2, decreased PH, hypoxia labs- blood tests, look for esinophils chest xray- usually it is normal initially but then hyperinflation, mucus plugging, air-trapping PFT- severely decreased peak flow FEV and FVC severely decreased FEV severely dimished RV increased FRC increased TLC increased Can't get air out due to high airway resistance tachypnea, tachycardia, increased BP, sweating profusely |
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Describe the treatment for asthma
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- avoid trigger
- avoid stress - prophylactic drugs- Intal (Cromolyn Sodium) prevents mast cell degranulation prior to an attack - bronchodilators: inhaled or systemic (aminophylline) Theodur, theo-aire, theophylline - steroids systemic: prednisone, hydrocortisone, inhaled: vasurel (beclomethasone), flovent - O2 - bronchial hygiene: hydration, CPT, PD & P - heliox 80% He and 20% O2 -psychological support |
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Define and state etiology for bronchiactasis
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a disease characterized by permanent bronchial dilation due to weaknes and damage to the bronchial wall
etiology: secondary effect due to a complication of some other pulmonary pathology -repeated pneumonia -childhood pneumonitis w/ pertussis -bronchial obstruction: tumor, foreign body -kartagener's syndrome: mucovicidosis w/dextrocardia and paranasal sinusits - repeated bronchitis |
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describe the pathophysiology of bronchiactasis
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destuctive changes to the airway wall structure. Destruction of smooth muscle tissue and bronchial wall cartiledge. squamous cell metaplasia. cartiledge rings breakdown and get floppy.
1- cylindrical- breaks down all around the cartiledge ring in the bronchi 2- fusiform- partial breakdown - area or patch affected 3- sacular- a sac forms. mucopurulent necrosis |
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list the tx for bronchiactasis
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cant rebuild the cartiledge
but can... treat infection treat primary problem Postural drainage bronchial lavage O2 therapy hydration surgical resection - remove sacular, patch stent bronchidlators and steroids - limited affect dont do percussion or IPPB |
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PFT for bronchiactasis
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decreased flows (distended a/w)
decreased FVC severe hypoxia due to v/q mismatch |
