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WAKA patho2
| Question | Answer |
|---|---|
| Eupnea is normal breathing that is rhythmic and effortless. RATE= 8-16 breaths/min. TV= 400-800 mL. T or F | TRUE |
| DYSPNEA is the objective sensation of uncomfortable breathing, the feeling of not being able to get enough air. T or F | false |
| What is hyperpnea? | (KUSSMAUL RESPIRATIONS) is characterized by slightly INCREASED rate, very LARGE tidal volumes and NO expiratory pause. |
| OBSTRUCTED BREATHING occurs when the airways are OCCULDED (COPD)! • CHARACTERIZED by SLOW RATE, LARGE TIDAL VOLUMES, INCREASED EFFORT AND PROLONGED INSPIRATION OR EXPIRATION. T or F | True |
| RESTRICTED BREATHING | results from STIFFED lungs or CHEST wall→ DECREASE compliance → SMALL TV and tachypnea. |
| CHEYNE-STOKES RESPIRATIONS | results from any condition that slows blood flow to the brain stem and is CHARACTERIZED by apnea lasting 15-60 seconds. Followed by ventilations INCREASING in volume until a peak is reached and then TV DECREASES again to APNEA. |
| COUGH | EXPLOSIVE EXPIRATION |
| HEMOPTYSIS | coughing up of BLOOD or BLOODY SECRETIONS |
| CYANOSIS | is the bluish discoloration of skin, sclera, and mucous membranes |
| CLUBBING | is the SELECTIVE bulbous enlargement of the DISTAL segment of a digit. It is painless and usually associated with LOW oxygenation |
| Defines as a _________ and ___________ disease characterized by airflow limitation, not fully reversible, progressive and associated with abnormal response to noxious particles or gases. | preventable and treatable. |
| Is COPD fully reversible? T or F | True |
| The damage involved in COPD is anatomical? T or F | True |
| COPD results from ________ or _________. most of the time both | bronchitis; emphysema. |
| COPD is disease resulting from the combination of acute bronchitis and pulmonary emphysema. T or F | False |
| COPD is characterized by difficult inspiration. T or F | False |
| Expiration is a passive process? T or F | true |
| Chronic Bronchitis defined as a hyposecretion of mucous and chronic productive cough. T or F | False; hypersecretion. |
| What is the criteria for chronic bronchitis? | At least 3 months of the year for at least 2 consecutive years. |
| Chronic bronchitis incidence is increasing or decreasing in smokers? | Increasing |
| The incidence of chronic bronchitis seen even more so in workers exposed to __________? | air pollution |
| Chronic is an infection? inflammation is secondary. T or F | False |
| In Chronic bronchitis there is an _________ thicker mucus production together with an ________ ciliary function. Causing a ________ in mucus secretion. | increased; impaired; decrease |
| In chronic bronchitis, bronchial walls become _________and thicker (edema + accumulation of inflammation cells) progressing from larger bronchial to ALL airways which become obstructed and eventually close, particular during expiration. | Inflamed and thicker |
| In chronic bronchitis the airways collapse late in expiration, trapping gas in the distal portions of the lung. T or F | False; early |
| The early collapse of airways on expiration lead to what 3 things? | Ventilation-perfusion mismatch, hypoventilation, and hypoxemia |
| What are the clinical manifestations of Chronic Bronchitis? | dyspnea, decreased exercise tolerance, wheezing, productive cough, and evidence of airway obstruction (decreased FEV1) in spirometry. |
| In Chronic bronchitis, FVC and FEV are __________ and the FRC and RV ________ as airway obstruction and air trapping become more pronounced | decreased; increased. |
| In chronic bronchitis patients will have afternoon toilette sputum and cough. T or F? | False; morning. |
| Diagnosis of chronic bronchitis is based on? | physical exam, chest x-ray, pulmonary function tests and blood gas analysis. |
| What is the best treatment for chronic bronchitis? | Prevention (stop smoking and pollution exposure). |
| Pathological changes in chronic bronchitis are reversible? T or F | False: irreversible |
| What is the pharmacological treatment for chronic bronchitis? | Bronchodilators and Expectorants. |
| Secondary infections associated with chronic bronchitis are treated aggressively and high-flow oxygen is administered to maintain peripheral P02 between 50 and 60 mmHg. T or F | False; low flow |
| Acute bronchitis is an acute infection or inflammation of the airways or bronchi commonly following a bacteria illness and is usually self-limiting? T or F? | False; viral |
| Acute bronchitis is self-limiting. T or F | True |
| Acute bronchitis will be maintained in the bronchi and not extend to the lobes. No pneumonia. Sometimes bacterial. Bacterial is better than viral. T or F | false; worse |
| Which of following is not a clinical manifestations of acute bronchitis: fever, chills, asthenia, anorexia, cough, or xerostomia? | xerostomia |
| In acute bronchitis there is a productive cough and mucus production? T or F | dry cough and no mucus production. |
| In the cases of bacterial acute bronchitis there is a productive cough, fever, and retrosternal pain. T or F | True |
| Bacterial infections related to acute bronchitis are rare in healthy adults but are common in patients with COPD. T or F | true |
| What is the treatment for viral acute bronchitis? | Rest, aspirin, humidity, and a cough suppressant |
| What is the treatment for bacterial acute bronchitis? | rest, aspirin, humidity, and antibiotics. |
| Pulmonary Emphysema is a __________enlargement of the gas-exchange airways accompanied by destruction of alveolar walls. | Permanent |
| In pulmonary emphysema, alveolar wall damage increases or decreases the area for gas exchange without fibrosis. | decreases |
| Pulmonary emphysema is secondary to chronic bronchitis and __________. | cigarette smoking |
| Clinical manifestations of pulmonary emphysema? | dyspnea on exertion progressing to dyspnea at rest. No cough with little sputum production. Tachypnea with prolonged expiration. |
| The disease course of pulmonary emphysema is prolonged with increased dyspnea and episodes of infection leading to LHF (Cor pulmonale) and death. T or F | False; RHF |
| Ultimate goal of pulmonary emphysema? | Prevent progression of the disease. |
| Diagnosis of pulmonary emphysema by simple chest x-ray will show what? | Flattened diaphragm and overdistended translucent pulmonary fields. |
| In pulmonary emphysema the vertical diaphragm and ribs are increased? T or F | false; horizontal. |
| Pulmonary function tests for pulmonary emphysema indicate? | Obstruction to gas flow during expiration. |
| Treatment for pulmonary emphysema is focused on minimizing air trapping and relieving dyspnea by relaxation and reconditioning exercises and breathing retraining exercises. T or F | TRUE |
| Asthma is an allergic condition and infectious. T or f | False. non-infectious |
| Bronchial asthma is a chronic infection disorder? T of F | False; inflammation |
| Characteristics of bronchial asthma are? | hyperresponsiveness of the airways and episodic periods of bronchospasm, involving biochemical, autonomic, immunologic, infectious (secondary), endocrine, and psychologcial factors in varying degrees |
| 50% of asthma cases develop during adulthood? t or f | false; childhood |
| 33% of asthma cases happen during adulthood before age of 40. T or fa | true |
| What is an asthma attack? and what are the causes? | Bronchospasm and caused by food, allergens, and emotions. |
| What are the classifications of asthma? | Extrinsic (allergic or atopic) and intrinsic |
| Extrinsic pathway of asthma is characterized by? | Mast cell activation and eosinophil infiltration which are triggered by environmental antigens. |
| Extrinsic pathway is mediated by? | IgE antibodies causing mast cells degranulation and release of inlfammatory mediators. |
| The intrinsic pathway is non-atopic or atopic, results from a previous infection? | non-atopic |
| Which of the following does not cause the intrinsic classification of asthma: respiratory tract infections, drugs, exercise, stress, allergens, cold, or dry air? | Allergens. |
| Clinical manifestations of asthma result from | bronchial smooth muscle spasm, increased vascular permeability (edema) and production of thick mucus and impaired ciliary function (airway obstruction). |
| Signs and symptoms of asthma include? | dyspnea, wheezing, sensation of chest constriction, non-productive cough, prolonged expiration, tachycardia, tachypnea. |
| Diagnosis of asthma is made through physical examination, absolute count of ___________in peripheral blood and spirometry. | Eosinophils |
| Treatment of asthma is elimination of the precipitating factors and agents. T or F | True |
| Acute episodes of asthma are treated with all of these drugs EXCEPT: bronchodilators, anti-inflammatory drugs, antibiotics, steroids, mast cell stabilizers? | antibiotics |
| The main problem of bronchial asthma is the progression to __________emphysema. | pulmonary |
| For adults with asthma, do we give steroids or adrenaline? | steroids |
| Pulmonary hypertension is established when the mean pulmonary artery pressure is above____mmHg at rest or ____ mmHg with exercise. | 25;30 |
| Pulmonary hypertension can be idiopathic (not common) or secondary to respiratory or CV disease causing an decreased volume or pressure in the blood entering to or remaining in the minor circulation or narrowing of occulusion of the pulmonary arteries.t/F | False; increased volume |
| Clinical manifestations of pulmonary hypertension are? | fatigue, dyspnea, chest discomfort, tachypnea, RV hypertrophy |
| Treatment for pulmonary hypertension is? | elimination of the primary disease before development of hypertrophy/fibrosis/irrversible thickness of the vascular medial smooth muscle layer. Palliative measures are relieve the symptoms and signs. Doesnt solve the problems but helps the patient. |
| PHTN is characterized by endothelial dysfunction with overproduction of what vasoconstictors? | thromboxane and endothelin |
| PHTN is characterized by endothelial dysfunciton with decreased production of what vasodilators? | NO and prostacyclin |
| The endothelial dysfunction results in vascular changes producing | fibrosis and thickening of the vessel wall, narrowing of the vessel lumen, and abnormal vasoconstriction. |
| for PHTN, vasoconstriction causes | increased pulmonary vascular resistance leading to increased pulmonary artery pressure-->increased RV afterload--> increased RV workload--> RV dilation--> RV hypertrophy--> RV failure |
| What is the catastrophic complication of the pulmonary HTN is_______resulting from LV CHF when the LV cant pump properly. | pulmonary edema |
| Pleural process involves? | serous covering of the lungs (pleura short cavity filled with fluid) and usually consists of accumulation of air, blood, serum or any other fluid in the pleural space. |
| pleural process is irreversible and hard to treat. t or f | true |
| Pleurisy | is the inflammation of the pleura causing it to become reddened and covered with exudate of lymph, fibrin, and cellular elements usually leading to pleural effusion. |
| The patient with pleurisy will present with? | chills, fever, pain on inspiration with a pleural friction rub hear over the affected area. PAIN IS THE HALLLMARK! happens as a secondary conditions to infectious agents. |
| Pleural effusion | Is the presence of fluid in the pleural cavity (blood, serum) due to different pathological processes. |
| The pathological processes involved with pleural effusion | lung cancer, pulmonary TB, CHF, and hypoproteinemia) |
| Pleural effusion and hypoproteinemia. | the low concentration of proteins reduces the oncotic pressure and water cannot be maintained inside the vessels--> compresses vessels |
| Pleural effusion may cause compression atelectasis and displacement of the _________content. | mediastinal |
| If pleural effusion is causing impairment of pulmonary function,________may be performed to drain the fluid from the pleural space. | thoracocentesis |
| Empyema | presence of pus in the pleural cavity, usually a complication of respiratory infection. |
| the patient with empyema will present with | fever, CYANOSIS, tachycardia, COUGH, and pleural pain |
| Treatment of empyema? | similiar to pneumonia and harder to drain and need aggressive antibiotic treatment. |
| Pneumothorax | is the presence of air or gas in the pleural space due to a rupture in the VISCERAL pleura or PARIETAL pleura and chest wall |
| Spontaneous (primary) pneumothorax | visceral pleura rupture showing SUDDEN and INTENSE, PLEURAL PAIN, tachypnea and DYSPNEA. |
| Secondary pneuomothorax | caused by CHEST TRAUMA (parietal pleura), surgical procedure rupture or a large bull (COPD) or mechanical ventilation (PEEP) |
| Clinical manifestations of secondary pneumothorax | similiar to those of spontaneous pneumothorax. VERY INTENSE PAIN. STABBING LIKE FEELING. |
| ARDS is a fulminant form of ___________ __________ characterized by acute lung inflammation and ____________injury due to numerous unrelated causes like sepsis and multiple trauma. | respiratory failure; diffuse alveolorcapillary |
| unrelated injury in ARDS are all but one.: PNEUMONIA, BURNS, ASPIRATION, cardiopulmonary bypass, infection, PANCREATITIS, blood transfusion | infection |
| What is the current mortality rate among people YOUNGER than 60 years is? | 40% |
| What is the current mortality rate among people older than 65 years is? | 60% |
| What is the most characteristic feature of ARDS? | increase capillary membrane permeability |
| In ARDS, the inflammatory response is mostly mediated by? | neutrophils, complement system, endotoxin, and tumor necrosis factor |
| ARDS will have ______blood flow to lungs and ________ v/Q | decreased; abnormal |
| in ARDS membranes are not intact thus what leaks from the capillary bed into the pulmonary instersitium and alveoli | fluid, proteins, and blood cells |
| In ARDS, hyaline membrane forms and fibrosis progressively obliterates the alveoli, respiratory bronchioles and interstitium leads to? | DECREASED FUNCTIONAL RESIDUAL CAPACITY AND R-->L shunt |
| Clinical manifestations of ARDS? | RAPID, SHALLOW BREATHING, respiratory alklalosis, marked dyspnea, decreased lung compliance. REFRACTORY HYPOXEMIA, and BILATERAL DIFFUSE ALVEOLAR INFILTRATION |
Created by:
jmenzrn
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