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41 Cards in this Set
- Front
- Back
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Obstructive Pulmonary Disorder
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1. Asthma*
2. Chronic Bronchitis * 3. Pulmonary emphysema* 4. Bronchiectasis 5 Cystic Fibrosis -all limit air flow |
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Asthma
-etiology -extrinsic -intrinsic -parasympathetic & sympathetic NS |
-Reversible, bronchospam, inflammation, increased airway secretions
-etiology: hypersensitivity of the tracheobronchial tree to various stimuli -extrinsic: pollen, dust mites, molds, milk -intrinsic: genetic? -para symp: bronchoconstriction, symp: bronchodilation |
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Asthma
2nd exposure, early response 10-20min |
antigen-antibody response inflammatory mediators released by mast cell IGE to specific receptors on mast cell
-prepares them for release of the inflammatory mediators during allergic rx. -immediate bronchoconstrition due to stimulation parasympathetic receptors -mucosal edema d/t increased vascular permeability -increased mucus secretions |
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Asthma
2nd exposure, late response 4-8hrs |
-reaches max in few hrs but can last days/wks.
-inflammatory mediators from mast cells, macrophages, epithelial cells -these substances induce other inflammatory cells wich produce epithelial injury and edema, retention of secretions -airway obstruction and air trapping behind secretion |
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Asthma
Clinical Manifestation (sign/symp) |
sudden dyspnea, expiratory wheezing, dry cough, progressive hyperinflation
-Ach cause muscle to contract, bands around bronchiole tightesn down -V does not = Q -hypoxemia, hypercapnia -use accessory muscles to breath -distant breath sounds -fatigue: work hard to breath -anxiety / apprehension |
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Asthma
diagnosis |
-Peak expiratory flow rate (PEF)
-Forced expiratory volume in 1 second (FEV1) -record personal best as baseline -do readings frequently for preventative care |
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COPD
-chronice bronchitis -Emphysema -risk factors |
group of respitory disorders characterized by chronic and recurrent obstruction of airflow in pulmonary airway
-leading cuase of morbidity & mortality worldwide -host/environment: smoking, hereditary deficiency in a1-antitrypsin, asthma, airway hyperresponsiveness |
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Chronic Bronchitis
-what is it -etiology -risk |
-chronic excessive mucous production and excretion into bronchial tree
-etiology: cigarette, industrial air pollution -edema, hyperplasia of submucosal glands -chronic cough (productive) for 3 month and 2 years consecutively -virus and bacterial infections -middle age men |
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Chronic Bronchitis
pathogenesis chronic inflammation |
1. hypertrophy of bronchial mucosal glands
2. goblet cells increase in number and size 3. inflammatory changes 4. loss of cilia 5. altered function of alveolar macrophages -mismatch v/q -unable to compensate by increase v = cyanosis and hypoxemia -good medium for organisms |
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Chronic Bronchitis
clinical manifestations (sign/symp) |
"Blue Bloaters"
-productive cough, -frequent respiratory infections -early dyspnea on exertion (DOE) -Prolonged exhalation -wheezes and crackles (fluid) -Hypercapnea (CO2 > 50): chronic respiratory acidosis w/metabolic comp. -Hypoxemia (O2 < 60): cyanosis, pulmonary hypertension -Cor pulmonale -increased erythropoietin polycythemia |
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2nd pulmonary hypertension
-etiology -pathogenesis |
-eleveated pulmonary atery pressure
-etiology:chronic low O2 < 55 -pathogenesis: vasoconstriction, d/t other disease cardiac or pulmonary) -2nd causes: increased pulmonary venous pressure, increased pulmonary blood flow & vascular obstruction -hypoxemia -shunts good short term but bad long term -rt heart catheter measures ABG |
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Cor Pulmonale
-clinical manifestations |
-right sided heart failure
-clinical manf: peripheral edema (back up of fluid into the venous system) -ascites: accumulation of fluid in pleural cavity -heptomegaly (larger liver) -plethera: redness of skin d/t polycythemia, warm moist skin -drowsiness, altered consciousness |
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Emphysema
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-anatomic alteration in the lung parenchyma characterized by abnormal enlargement of alveoli & alveolar ducts, destrcution of alveolar walls
-loss lung elasticity -leads to hyperinflation and increased TLC (total lung capacity) |
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Emphysema
etiology |
etiology: alpha1-antiprotease deficiency
-autosomal recessive disorder -smoking -aging -air pollution -recurrent infection -permanent once change in tissue structure -leads to impaired gas exchange |
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emphysema
clinical manifestations (sign/sypm) |
"Pink Puffers"
-purse lipped breathing -early dyspnea -thin, barrel chest -increased lung capacity & residual vol. -diminshed breath sounds -proportionate loss of V/Q -able to overventilate = pinkpuffer = normal ABG (until late in disease) -prominent use of accessory muscles, over distention of ribs -lose lung elasticity -hyperinflate lungs -eating difficult, use all energy to breathe |
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Cystic Fibrosis aka mucoviscidosis
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-autosomal recessive of chromosome 7
-apocrine sweat glands, increased Na -pancreatic exocrine glands deficiency -decreased production of cystic fibrosis transmembrane conductance regulator (CFTCR) -CFTCR: function as Cl- channel in epihelial cell membranes -chronic disease in children -fluid secretion in exocrine glands of epithelial lining of the respiraty, GI, repordutive tracts |
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Cystic Fibrosis
pathogenesis |
-CFTCR deficiency leads to decrased cl transport leads to increased cellular reabsorption of Na and H2O leads to increased viscosity of secretions
-leads to obstructed airways and recurrent pulmonary infections |
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Cystic fibrosis
pathogenesis |
-originally chronic bronchiolitis & bronchitis
-after months,yrs structural change in bronchial wall = bronchiectasis -impairment of mucocillary function -destruction of lung tissue -impaired gas exchange and frequent infections -on antibiotic all the time -bacteria becomes resistent to large amts antibiotics |
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cystic fibrosis
Pathogenesis -apocrine sweat gland -GI tract |
gland: increase cl concentration in sweat,+ sweat cl test (diagnosit tool)
GI: increased viscosity of secretions, poor nutrient absorption pancreas: viscous obstrction of exocrine glands, plugging & obstruction, fibrosis of the pancreas, decreased excretion of pancreatic digestive enzymes -steaorhea (fatty stool), diarrhea, abdominal pain -8% diabetits -high colorie intake, work to breath + high metabolism of disease |
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Cystic fibrosis
clinical manifestations |
-6-12mths of age diagnosed
-recurrent resp. infections, malabsorbtion, failure to thrive -respiratory: persistent cough, frequent pulmonary infections, barrel chest, clubbing of fingers -GI: oily stools, malnutrition |
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Cystic fibrosis
diagnosis |
-sweat chloride test
-slow progressive decline -pancreatic: diabetes -complications: resp. infection -early diagnosis important get on right tx. |
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Pulmonary embolism
-etiology -risk |
-perfusion disorder: blood born substance lodges in branch of pulmonary artery & obstructs flow (perfusion)
-etiology: DVT (most common), amniotic fluid, fat (femur fracture), malignant tumors, air, vegetations risk: immobility, orthopedic & gynecologic surgery, birth control ((hormone-ability to anticoagulate), cancer, pregnancy (hormone) -unsuspected until embolism occurs |
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Pulmonary embolism
-pathogenesis |
-venous embolus goes to right side of heart, lodges pulmonary arteriol or capillary, mechanical obstruction
-15-7% mortality |
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Pulmonary embolism
-clinical mnifestations |
-sudden unexplained dyspnea
-chest pain -hypoxia w/o tachycardia -restlessness -sudden death (massive emboli) -low BP -rapid weak pulse |
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Pulmonary embolism
-diagnosis |
-v/q scan: radiolabeled albumin injected in IV, radiolabeled gas inhaled (not definitive due to change in breathing)
-spiral CT (helical angigraphy) scan: tricky due to hypersensitivty, need to be adequately hydrated if not = renal failure, detect emboli in proximal pulmonary artieries -increase D-dimer: measure plasma d-dimer degraduation product of coagulation factors activated as a result of thrombembolic event, not good test if have lung disease |
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Respirtory Failure
-etiology |
-o2 <60, CO2 > 50 (in absence of chronic lung disease)
-etiology: v/q mismatch (high/low) -shunt -impaired diffusion |
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V/Q mismatch
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-low v/q <1 = perfusion w/o ventilation
-high v/q >1 = ventilation w/o perfusion (ie pulmonary embolism) -reductin V by 1/2 cuases CO2 to double = hypoventilation |
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hypoventilation low v:q
-etiology |
-reduction in vol. of fresh air in alveoli
-etiology: narcotic/sedative OD, neuromuscular disorders (problem inervateing muscle) = Guillain-Barre-subacute polyneuropathy ifiltration of mononuclear cells around capillaries of peripheral neurons, edema of endocneurial compartment with 80-90% spontanoues recovery, also Muscular Dystrophy, chest wall abnormalities -hypercapnic resp. failure -decrease depth, decrease rate |
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hypercapnic respiratory failure
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-increase co2 in arteries
-asthma, COPD, cystic fibrosis, CNS disorders -ventilatory failure = COPD -alveolar hypoventilation -normal is carbonic acid 1 : bicarbonate 20 |
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Hypercapnic Resp. failure
-clinical manifestations |
-resp. acidosis: ph less than 7.35, CO2>45
-vasodilation: headache, increased intracranial pressure, conjunctival hyperemia, flused skin -mental confusion: co2 narcosis, somnolence leads to disorientation leads to coma -moderate decrease 02 |
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Shunt
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blood is not exposed to O2
-intrapulmonary -anatomic: ventricular-septal defect (opening in ventricular septum results from an imperfect separation of the ventricles during early fetal dev. |
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diffusion limitation
-etiology -classic symp |
-destruction or thickening of the alveolar-capillary membrane (V/Q=1)
-etiology: pulmonary edema, interestial lung diease, recurrent pulmonary embolism -classic symp: hypoxemia with exercise -thick membrane = gas can't move across |
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Monifestions of hypoxia/hypoxemia
-general -decreased 02 to brain -tissue hypoxia -compensatory |
-general: o2<50, prolonged expiration (1:3-1:4), retractions of chest wall, pursed lip breathing, cyanosis (late sign)
-O2 to brain: restlessness, combative, confusion -tissue hypoxia: fatigue, inable to speak w/o pause -compensatory: tachycardia, hypertension -compensate hypoxemia by increased V, pulmonary vasoconstriction, increase RBC production -hyperventialtion results from hypoxic stimulis of chemoreceptors |
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Acute Respiratory Distress Syndrome [ARDS]
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sudden progressive respiratory failure associated with damage to & increased permeability of the alveolar capillary membrane.
-acute lung injury, also children -becomes permeable to substances should not be |
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ARDS
-etiology -risk |
-etiology: direct or indirect lung injury
-risk: gram-neg sepsis, aspiration of gastric contents, major trauma, near drowning -sepsis 2nd to pulmonary or nonpulmonary infections -acure pancreaitis -hematologic disorders -metabiolic events -rx to drugs and toxins |
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ARDS
-pathogenesis |
-lung injury leads to diffuse epithelials cell injury leads to increased alveolar-capillary permeability & damage to alveolar type 2 cells
-increase permeability permits fluids plasma proteints , blood cells, move out of vascular compartment into interstitum and alveoli in the lung |
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ARDS
-pathogeneis (cont.) |
-increased alveolar-capillary permeability leades to movement of fluid & RBCs and proteins,leads to interstitial edema or alveoli, leads to shunt & impaired gas exchange
-end result profound hypoxia (very ill) -gas exhcange further comprimesd by alveolar collapse resuling from abnormalities in surfacant prodcution (premature infant) |
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ARDS
summary pathogenesis |
neutrophils acumulate: synthesize and release protlytic enzymes, toxic o2 species, phospholipid products that increase inflammatory response.
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ARDS
-clinical manifestations, early |
-correlates with multiple blood transfusions
-early: hours to 2days,dyspnea, tachypnea, cough and restlessness, clear lungs or fine crackles, mild hypoxemia, respiratory alkalosis, normal CXR |
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ARDS
Definiative clinical manifestations |
-hypoxemia: o2<50 on mechanicl ventilatory support
-chest xray: new bilateral interstitial & alveolar infiltrates (looks like cotton balls everywhere) -pulmonry hypertension -predispoing condition within 48hrs (initiating event, resp. distress) |
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ARDS
complications |
-nosocomial pneumonia
-barotrauma: positive pressure in lungs, spontanious pneumothorax leads to tension pneumothorax -stress ulcers -renal failure -lots of secretion parolytic illiac - gut goes to sleep -high metabolic needs |
