Pulmonary Path Flashcards

Question

Pleural Effusion S/S Dx and Rx

Answer 1

``` S/S: dyspnea, hypoxemia Dullness on percussion Absent breath sounds over affected area Dx: CXR Rx: diuretics Thoracentesis and fluid analysis Chest tube placement ```

Answer 2

S/S: pleuritic pain, SOB, ↑RR, ↓ breath sounds, crepitus Dx: CXR, ABGs Rx: Observation Chest tube insertion Surgical repair Pleurodesis – instillation of caustic substance

Answer 3

``` Compression by fluid, mass Obstruction by mucous plug Surfactant impairment Postsurgical S/S: ↑RR, ↑HR, fever, decreased breath sounds Dx: CXR Rx: Cough, HHN, bronchoscopy ```

Answer 4

Parasympathetic stimulation → bronchoconstriction | Sympathetic stimulation → bronchodilation

Answer 5

Chronic inflammatory airway disease characterized by hyper-responsiveness & bronchospasm Prevalence increasing, esp. children Hereditary components Familial history of allergy- predisposition to IgE mediated response to common allergens 100 genes associated with asthma: code for interleukins, leukotreines, etc. Environmental components – especially urban

Answer 6

Extrinsic Type I hypersensitivity response to extrinsic antigen Usually begins childhood Allergens: dust mites, animal dander, alternaria fungus Intrinsic Non-allergic mechanisms “bronchospastic triggers” Respiratory tract infection Exercise – mechanism unclear Inhaled irritants: cigarette smoke, pollution, cold air GERD Emotions: triggers spasm through vagal pathway

Answer 7

Unified airway hypothesis Allergens stimulate upper airways, trigger response in lower Allergen inhaled into hyper-responsive airway Release of interleukins B-cell activation, production of IgE Degranulation of mast cells on mucosal surface Release of histamine, prostaglandins, leukotreines Attraction of eosinophils, tissue damage ↑capillary edema, bronchospasm, mucous production ``` 2 phase response to allergens Acute response Release of histamine Bronchospasm main response Late response Migration of inflammatory cells hours later → Airway edema Bronchospasm Mucous production ``` ``` Eventual airway remodeling due to inflammation Thick, hyperresponsive Obstruction and hyperinflation Decreased perfusion Hypoxemia CO2 retention and respiratory failure ```

Answer 8

S/S: mild to severe Chest tightness Cough Wheezing Thick mucous Prolonged expiration – drop in PEF and FEV1 Severe attack: unable to speak, BS↓ or absent, cough ineffective, respiratory failure Status asthmaticus Severe prolonged attack refractory to usual treatment

Answer 9

Dx: PFTs w/wo bronchodilator Severe attack: ABGs, peak flow rate Treatment guidelines for children & adults Nonpharmacologic Education Self-monitoring with peak flow meter/spirometry PEF 80-100% of predicted = good control PEF 50-80% of predicted = insufficient control <50% = poor control Environmental control Identification & avoidance of triggers

Answer 10

Meds for longterm control and short acting for acute attacks Bronchodilators Short acting beta agonist(SABA) - albuterol Long acting beta agonist (LABA)- salmetrol Anticholinergics -ipratropium to block parasympathetic NS + fluticasone = Advair Anti-inflammatory agents Corticosteroids Cromolyn Leukotriene modifiers

Answer 11

National Asthma Education and Prevention Program, VaDOD Mild intermittent – sx < 2X week. No daily meds. Mild persistent – sx > 2X week. 1 daily med. Moderate persistent – daily sx. 1-2 daily meds Severe persistent – Daily meds plus steroids. Emergency: inhaled β2 agonist, s.q. epinephrine, solumedrol IV, supplemental O2

Answer 12

COPD – disorders characterized by chronic, progressive obstruction to airflow Emphysema – abnormal permanent enlargement of distal airways with destruction of alveolar walls Primary emphysema: inherited deficiency of α 1- antitrypsin Secondary emphysema: caused by smoking 99% of emphysema

Answer 13

``` Smoking → inflammation in small airways Infiltration of inflammatory cells Release of cytokines Elastase (enzymes) from inflammatory cells break down elastin within septa Loss of elastic fibers & alveolar tissue → destruction of septa Large hyper-inflated airspaces replace normal alveoli Bullae and blebs Centriacinar Panacinar ↓ surface for gas exchange ↓perfusion Loss of elastic recoil ```

Answer 14

``` Inflammation of bronchi from irritants and infection; chronic productive cough Main cause is cigarette smoking Pathophysiology Inspired irritants→↑mucous production Hyperplasia of goblet cells Impaired ciliary activity Infection develops Bronchial walls thicken from chronic inflammation & spasm Airways collapse in expiration, trapping air Excessive mucous production Decreased perfusion Hypoventilation Hypercapnea Hypoxemia ```

Answer 15

``` Pink Puffer Barrel chest Weight loss Dyspnea Cyanosis – late Cor pulmonale – late Polycythemia - late ``` ``` Blue Bloater Copious sputum Severe dyspnea Cyanosis Cor pulmonale Edema Polycythemia ```

Answer 16

``` CXR – diaphragm flat, distended lung fields ABGs: hypoxemia, hypercapnea 6 minute walk test How far can they go How many rests do they take What’s their pulse ox doing? PFTs ↓FEV1 (low) ↓FVC (don’t blow much air out) ↑ residual volume (a ton of air left in the chest) ↑ total lung capacity ```

Answer 17

``` Control of environmental irritants Nutritional support Exercise training, pulmonary rehab Breathing exercises Management of secretions Pharmacologic by the GOLD – Global Initiative for COLD) Bronchodilators, anticholinergics, steroids Oxygen ```

Answer 18

``` Autosomal recessive disease Mutation of CFTR gene Defective chloride transport Dehydrated, thick mucous Recurrent infection & inflammation ```

Answer 19

Dx: sweat test, genetic testing, newborn screening Pulmonary s/s: chronic cough, frequent pulmonary infections, hypoxia, SOB, clubbing of fingers, barrel chest Structural changes in Airways Bronchiectasis, permanent dilation of bronchioles Tx: control/treat infection, thin mucous, promote clearance, maintain nutrition, lung transplant

Answer 20

Diverse group of disorders which involve inflammation & fibrosis Occupational diseases, damage from drugs Lungs stiff, difficult to inflate Patho: inflammation →eventual fibrosis Alveolar macrophages secrete fibroblast growth factor PFT: ↓VC, ↓TLC, progressive hypoxemia

Answer 21

Most common interstitial lung disorder Most cases >60 Patho: inflammation and fibrosis, diffusion block, decreased compliance S/S: DOE, crackles Dx: PFTs, CT chest, lung biopsy Rx: steroids, cytotoxic drugs, transplant

Answer 22

Stop breathing for 10 sec. multiple times/night Disrupts normal ventilation and sleep patterns Central Sleep Apnea Rare, associated with brain dysfunction Obstructive Sleep Apnea Prolonged partial or intermittent complete upper airway obstruction during sleep

Answer 23

Adults Risk factors: obesity, more common in men s/s: loud snoring alternates with periods of silence, persistent daytime sleepiness Can develop hypoxia, dysrhythmia, systemic HTN, pulmonary HTN, increased MVAs Children 13% 3-6 year olds, 2-3% middle school Obesity, allergies/asthma, adenotonsillar hypertrophy s/s: snoring, enuresis, napping Cognitive/behavioral impairment CV disease, insulin resistance, decreased growth

Answer 24

``` Occlusion of part of pulmonary vascular bed by embolus Pathophysiology Deep venous thrombosis Thrombi travel up IVC Emboli may be single, multiple massive ```

Answer 25

Clots lead to an inflammatory reaction within the lung Mediators released – catecholamines, radicals Pulmonary vasoconstriction ↑ pulmonary P, RV strain V/Q mismatch ↓ surfactant production, atelectasis Large infarct → hypoxia and shock

Answer 26

``` “Classic” S/S: Sudden onset of pleuritic pain Tachypnea, dyspnea, tachycardia Hemoptysis Signs of DVT Pleural friction rub, anxiety Patient may be asymptomatic Dx: CXR normal until atelectasis occurs Helical CT V/Q scan, d-dimer, ECG – RV strain, ABGs ```

Answer 27

Mean PAP > 25 mmHg at rest Primary pulmonary HTN rare, affects young women Secondary pulmonary HTN Congenital heart disease Valvular heart disease Severe COPD HF Vasoconstriction & concentric intimal fibrosis Narrows, stiffens pulmonary arteries, arterioles Endothelial dysfunction ↑ vasoconstrictors, ↓ vasodilators ↓ prostacyclin (PGE2) Remodeling with narrowing, thickening, fibrosis Chronic ↑PAP → right HF

Answer 28

``` S/S: Fatigue, CP, dyspnea Right HF Dx: echocardiogram Right heart cath & drug study Rx: PH clinics Oxygen, diuretics, anticoagulants Pulmonary vasodilators: IV prostaglandins (Flolan) Remodulin Sildenafil, Beraprost, etc. ```

Answer 29

``` Diffuse injury to AC membrane Associated with trauma, shock, sepsis Patho: massive inflammatory response Neutrophils, platelets Mediators, oxidants Decreased surfactant Interstitial edema Hyaline membrane forms ```

Answer 30

``` S/S occur within hours of insult (shock, sepsis) Hyperventilation Severe hypoxemia Respiratory acidosis Dx: ABGs, CXR Rx: supportive Ventilatory support Low volume ventilatio ECMO ```