Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
404 Cards in this Set
- Front
- Back
|
What are the most common viruses responsible for Upper Respiratory infections
|
Rhinoviruses
Influenze Parainfluenza Coronavirus Adenovirus Respiratory Synctial Virus Enterovirus Rubella Varicella-zoster Epstein Barr |
|
|
What are some bacterial infections associated with Respiratory Infections
|
Group A beta hemolytic streptococcus
S. Pneumonia Hemophilus Influenza Moraxella Catarrhalis Staph Aureus Chalmydia pneumonia Mycoplama pneumonia |
|
|
When does the Lung become sterile?
|
Below the Stina
|
|
|
What are some chronic conditions that are important to be caught early
|
Allergic Rhinitis
Obstructive Process Autoimmune Disorders that present in the oropharynx Cancer |
|
|
Two major types of hearing loss
|
Conductive
Sensory-neural |
|
|
What is conductive Hearing Loss
|
Occurs from external or middle ear dysfunctions
Infection, effusion, sclerosis Disruption of the bones Cerumen |
|
|
What is the Weber test used for
|
Sound Lateralization
|
|
|
What is Sensory Hearing Loss
|
Deterioration of the cochlea - usually high frequency
|
|
|
Causes of Sensory Hearing Loss
|
Age, systemic diseases, head trauma, workers exposed to loud noises
|
|
|
What are diseases of the ear canal
|
carumen impaction
external otitis |
|
|
What is Otitis Media signs
|
redness of the ear drum
decreased mobility of the ear drum swelling and possible fluid behind the membrane |
|
|
what is the treatment of Otitis Media
|
Treatment is specific antibiotic therapy:
Amoxicillin Erythromycin plus a sulfonamide May use: Augmentin or cefaclor |
|
|
What is Vertigo?
|
Exaggerated sense of motion. Feel like they are falling or that the ground is rolling under their feet
Needs to be distinguished from syncope, imbalance and lightheaded |
|
|
What is the Romberg test?
|
A gait evaluation and complete ocular exam to look for lesions and nystagmus
|
|
|
What are some peripheral lesions?
|
Meniere's syndrom (endolymphatic hydrops), labrynthitis, positioning, traumatic or cervical vertigo, vestibular neuronitis and vertigo associated with migraine
|
|
|
What are central lesions of the ear?
|
Brainstem vascular disease, tumors, multiple sclerosis and migraine.
|
|
|
How to treat Meniere's Syndrome?
|
Low salt diet and HCTZ (50-100 mg daily)
|
|
|
Symptoms of Viral Upper Respiratory Infections
|
Most are nonspecific:
Headache, nasal congestion, watery rhinorrhea, nasal congestion, sneezing, sore throat, fever and general malaise No Localization to one area |
|
|
How long does Viral Upper Respiratory Infections last?
|
10-14 days with lessening symptoms in the final course of the illness
Acute, mild and short duration |
|
|
What is the nasal exam say with a Viral Upper Respiratory Infections last?
|
Red, edematous mucosa with discharge.
|
|
|
how do you treat Viral Upper Respiratory Infections?
|
Supportive Measurements. Antibiotics have no role in the treatment of viral upper respiratory infections.
|
|
|
What is the mainstay of treatment of Viral Upper Respiratory Infections?
|
Let the illness run its course:
Rest an Fluids Decongestants of saline nasal spray Anti-inflammatory agents Supportive patient education Instructions to follow-up if the symptoms localize, worsen or if systemic problems develops |
|
|
What is Sinusitis?
|
Inflammation involving the four paired structures surrounding the nasal cavities
|
|
|
What is the reason for the presentation and symptoms of sinusitis?
|
Retention of secretions secondary to inflammation or infection
|
|
|
How long does sinusitis last?
|
usually presentation after or in conjuction with an upper respiratory infection.
Acute: under 4 weeks or chronic more than 4 weeks |
|
|
Symptoms of Sinusitis?
|
Nasal Drainage and congestion
Facial pain or pressure headache Fatigue depression thick purulent postnasal discharge cough sneezing fever Tooth pain and halitosis may be present |
|
|
Signs of Sinusitis?
|
Fever
Pain on Palpation of the affected sinus Observation of purulent discharge in the narse o in the posterior pharynx Inability to transilluminate the sinuses |
|
|
Patients who are acutely toxic with Sinusitis
|
have high fever
obtunded in severe pain have localized signs of periorbital edema or signs of leakage into the brain NEED TO BE TREATED EMERGENTLY |
|
|
How is Treatment for sinusitis done?
|
based on etiology.
|
|
|
How to Treat Viral Sinusitis?
|
it is usually mild, has no purulent signs of obstruction and responds to saline nasal solutions,
antiinflammatories rest within 7 days |
|
|
What is Bacterial sinusitis
|
It is more painful and associated with obstruction of the sinuses and purulent discharge. Last for more than 7 days
|
|
|
How to treat Bacterial Sinusitis
|
Antibiotics - use for all 10 days
- Amoxicillin - 500 mg 3x a day - Bactrium DS - 2x daily - Cephalexin - Cefixime - Cipro - Augmentin - Levofloxin |
|
|
What about using X-rays with Sinusitis
|
Imaging is usually not recommended as the diagnosis can be made on clinical grounds alone.
If imaging is needed to rule out a chronic obstruction or an infection that does not respond to antibiotics use |
|
|
What is Allergic Rhinitis
|
Seasonal Rhinitis
Associated with other upper respiratory infections such as sinusitis and otitis media |
|
|
What is the pathophysiology of Allergic Rhinitis
|
Allergic response mediated by IgE antibodies
|
|
|
What are the 3 phases to the response of allergic response for Allergic Rhinitis?
|
Sensitization
Early Phase Late Phase |
|
|
What are cells that work to create symptoms of allergic rhinitis?
|
IgE antibodies
Mast Cells Histamines Leukotreines Cytokines are released in the late phase |
|
|
Classification of Allergic Rhinitis
|
Perennial and Seasonal
|
|
|
What is Perennial Allergic Rhinitis
|
Symptoms are experienced year round
Most common allergens: Dust mites, cockroach droppings, animal dander and mold |
|
|
What is Seasonal Allergic Rhinitis
|
Symptoms are Seasonal
Most Common allergens: Grasses, trees and weeds |
|
|
Symptoms of Allergic Rhinitisinates s?
|
Sneezing
Itching Rhinorrhea Congestion Mouth Breathing Postnasal discharge Excessive Tear Production Soreness of the eyes Fatigue Irritability Depression |
|
|
History of Allergic Rhinitis?
|
Seven qualities plus a medication history.
Environmental exposure is critical in making the right diagnoses, family history of allergies is also critical |
|
|
Physical Presentation of Allergic Rhinitis?
|
Nasal turbinates swollen and coated with clear exudates
mouth breathing due to obstruction of nares "allergic shiner" |
|
|
Diagnostic Testing of Allergic Rhinitis?
|
Skin Testing: intradermal and prick
RAST Testing: |
|
|
Teatment of Allergic Rhinitis?
|
Minimize the exposure to the allergens
Prevent and/or ameliorate allergy symptoms with pharmacologic agents Alter the immune response with immunotherapy Work with the patient during all phases of treatment |
|
|
Pharmacologic agents with the treatment of Allergic Rhinitis?
|
Antihistamines
Intranasal corticosteroids |
|
|
What is acute pharyngitis/tonsillitis caused by?**
|
Due to viral infections but attention should be paid to group A beta hemolytic streptococcus (GABHS) which can progress to acute rheumatic fever and acute glomerulonephritis
|
|
|
What accounts for most cases of pharyngitis?
|
Rhinoviruses and coronoviruses
|
|
|
What viruses can present with acute pharyngitis?
|
HSV, cocksackie virus A, CMV, EPV, HIV
|
|
|
Signs and Symptoms of Pharyngitis?
|
Tender cervical adenopathy,
pharyngeal exudates, possible fever, myalgias, headache and cough |
|
|
Should exudates that present with pharyngitis and tonsilitis be cultured?
|
Yes.
Any pharyngitis that presents with vesicles on the pharynx may be HSV or cocksackie |
|
|
What should you do if GABHS is suspected?
|
Rapid Strep test
It is negative do a culture and send it off Rapid strep test are highly sensitive but not highly specific |
|
|
What is the management of pharyngitis?
|
The Centor Criteria:
- Fever over 38 degrees C - Tender cervical adenopathy - Lack of cough - Pharygotonsillar exudate |
|
|
Treatment paths when using the Centor Cirteria?
|
- Test all patients who satisfy 2 or more of the Centor criteria and treat only those with positive results
- Test those who satisfy 3 or more of the Centor criteria and treat both those with positive and thos who have all four criteria - Test nobody and treat all who satisfy 3 or 4 of the Centor Criteria |
|
|
How to treat GABHS?
|
- Penicillin V
- Cephalexin - Erythromycin |
|
|
What does Mononucleosis present with?
|
Marked Lymphadenopathy and shaggy white-purulent tonsillar exudate, fever and malaise
|
|
|
What is Mononucleosis caused by?
|
- Epstein-Barr virus
- Can test for the virus using and ELISA test - Group A strep can co-exist with Mono |
|
|
What do you need to watch for with Mono?
|
Even through it is self-limiting you need to watch for airway obstruction, hepatosplenomegaly, Chronic E-B virus
|
|
|
What drug should you avoid with Mono?
|
Amoxicillin because they will develop a rash
|
|
|
What is Laryngitis?
|
Any inflammation involving the larynx
|
|
|
What is laryngitis characterized by?
|
Hoarseness
Reduced vocal pitch or aphonia usually associated in association with upper respiratory infection illness |
|
|
How do you treat Laryngitis?
|
Treat as Upper Respiratory Infection unless severe swelling is suspected of lesions is suspected
|
|
|
What do you do if Laryngitis is not responding to treatment as an infection?
|
They need to be scoped
|
|
|
How is Croup characterized by?
|
Acute and predominately viral infections are characterized by marked swelling of the subglottic region of the larynx
Usually occurs children under 6 and is predominately viral in origin |
|
|
What is epiglottitis?
|
Acute rapidly progressive cellulitis of the epiglotitis and adjacent structures that can result in complete and sometimes fatal airway obstruction in both children and adults
|
|
|
Why don't you mess around with the epiglottitis?
|
Trigger happy and if it is touched the airway is closed off
|
|
|
Most common Etiology of epiglottitis?
|
Hemiphilus influenza
- but with the introduction of HIB vaccination other pathogens can be responsible (Streptococcus, S. pneumonia, Hemophilus parainfluenza and Staph aureus) - Viruses have not been established as entities causing epiglotittis |
|
|
What is the presentation of Epiglottitis?
|
Very Toxic and rapid in onset
- High fever - Severe sore throat - tachycardia - dyspnea - drooling - sitting forward to breathe - acute respiratory distress - Inspiratory stridor - Retraction of the chest wall |
|
|
What does the oropharygeal exam reveal in epiglottis?
|
midly red throat, less than would be expected of the symptoms seen by the clinician
|
|
|
Why don't you visualize the posterior pharynx with a tongue blade?
|
cause an acute larygospasm that will cause a total airway obstruction
|
|
|
Treatment of Epiglottitis?
|
Emergent
- Patients need to have their airway protected, usually in the ICU until antibiotic treatment takes effect. - Patients are hospitalized and placed on watch for airway obstruction - Laryngoscopy with plans for possible intubation is indicated to obtained cultures from the epiglottis and confirm the diagnosis |
|
|
What are the antibiotics used in epiglottitis?
|
Include 2nd or 3rd generation cephalosporin, ampicillin/sulbactam, clindamycin and bactrim for those allergic to PCN
|
|
|
What are some other upper respiratory conditions?
|
- Benign nasal tumors: polyps, papillomas
- Malignant nasopharyngeal tumors - Lymphoma, Sarcoidosis, Wegner's Granulomatosis - Ulcerative Lesions |
|
|
What is Idiopathic Pulmonary Fibrosis?
|
Interstitial lung disease
|
|
|
What is Idiopathic Pulmonary Fibrosis characterized?
|
Chronic Inflammation, accompanied by an uncontrolled healing response that causes progressive scarring or thickening of tissues between of the lung's alveoli or air sacs
|
|
|
What is the cause of Idiopathic Pulmonary FIbrosis?
|
It is unknown
- although the body's own immune response seems to play a major role |
|
|
What do people with Idiopathic Pulmonary Fibrosis present with?
|
- Subtle onset of breathlessness with exercise.
- Overtime there is a progressive worsening of breathlessness, as oxgen transfer to the blood decreases - Right sided heart failure often develops - Median survival is 5 years |
|
|
What are fibrotic disorders?
|
Large group of disorders affect alveolar wall and interstitium leading to diffuse scarring
- fibrosis - restrictive lung disease, diffusion defects - >130 Diff. Disease |
|
|
Common Pathology of Fibrotic Disorders?
|
Inflammation - infiltration by various pathogens
- Macrophages - Lymphocytes - Neutrophils - Plasma Cells |
|
|
What what Associated Granuloma?
|
Mass of nodular tissue composed of capillary buds, fibroblasts, localized collection of phagocytic type cells resulting from inflammation and injury
|
|
|
What is the Key Feature of Associated Granuloma?
|
Disordered Repair
|
|
|
How does Associated Granuloma show up on X-ray
|
Shows that it is fibrosis and Honeycombing on the X-ray
|
|
|
What are the 2 classifications of Associated Granuloma
|
Lymphocitic
Neutrophilic |
|
|
What is Lymphocytic Associated Granuloma?
|
Granulomatous features initial exposure to antigens - sometimes unknown
|
|
|
What is Neutrophilic Associated Granuloma?
|
Antigen/antibody complexes activate macrophage with release factors attracting neutrophils
- Produce Chemical mediators toxic to Alveolar wall |
|
|
What is the patho-physiology of Associated Granulomas?
|
- Decreased Compliance
- Decrease Lung Volumes - Impaired Diffusion - (KEY FEATURE) - Eventual Pulmonary Hypertension - Fibrosis irreversible - Alveolitis - Tx Steroids |
|
|
Diagnosis of Associated Granulomas?
|
- History
- Biopsy needed to establish specific diagnosis |
|
|
What is the etiology of Associated Granulomas?
|
- Affects both sexes equally world-wide
- Most Frequent in 40-60 y.o - Familial occurence |
|
|
What is the key feature that causes Associated Granulomas?
|
Inhalation of particles
- more than 8 microns can't get into lungs - Less than 0.5 microns enter and leave like gas - 1-5 microns are most likely cause - Also need to look at: Type of particle, Duration and intensity of exposure and smoking history |
|
|
What are some agents that cause Associated Granulomas?
|
- Organic Dusts
- Inorganic Dusts - Noxious gases - Soluble aerosols - Micro-organisms: bacteria/parisites |
|
|
What is Cryptogenic Pulmonary Fibrosis?
|
- Idiopathic Pulmonary Fibrosis
- Non-specific - Characterized by Chronic inflammation - Progressive fibrosis of alveolar wall |
|
|
Primary idiopathic disease is part of?
|
Systemic connective tissue disorders
- Example: Rheumatoid Arthritis, Lupas or erythematosus |
|
|
What are pathogens used from Cryptogenic Pulmonary Fibrosis?
|
Appears to be immune mechanism of inappropriate antibody production
|
|
|
What is the Clinical Presentation of Cryptogenic Pulmonary Fibrosis?
|
- Dyspnea of Exertion
- Nonproductive Cough - History of Arthralgia - As Progresses - get fatigue - Anorexia/weight loss - Fine end - Inspiratory rales at base - Clubbing - Cor Pulmonale - Not a Blue Bloater of Pink Puffer |
|
|
What is the Hammond-Rich Syndrome?
|
- Occasionally rapid progression and deterioration
- Less than 6 months |
|
|
Pathophysiologt of Chronic Fibrosing Alveolitis?
|
PFT
- Restrictive - decrease lung volumes - Decrease Clt - Have a diffusion defect - (large A/a gradient) - Chronic Low PCO2 - No O2 in no CO2 out |
|
|
Treatment of Chronic Fibrosing Alveolitis
|
Supportive, relentless downhill course
- Possible steroids - O2 |
|
|
What is Sarcoidosis?
|
Systemic disease characterized by non-caceating granuloma in affected organs
- Lungs, Liver**, Eye, skin, spleen |
|
|
Etiology of Sarcoidosis?
|
More common in blacks than whites,
More in Female than Men 20-40 year olds Etiology unknown |
|
|
Pathology of Sarcoidosis
|
Diffuse non-caseating granulomas in parenchyma, bronchial wall submucosa
|
|
|
Clinical Presentation of Sarcoidosis?
|
Expertional Dyspnea
May be asymptomatic at diagnosis X-ray Fever Weight loss Malaise |
|
|
X-Ray with Sarcoidosis?
|
Diffuse interstitial Pattern
- Enlarge hilar, paratracheal lymph nodes - ****Bilateral Hilar adenopathy (butterfly pattern)*** |
|
|
Pathophysiology of Sarcoidosis
|
PFT
- May be combined restrictive or obstructive - Decrease TLC Decrease in Diffusion - Many also decrease expiratory flows Decrease compliance Hypoxemia |
|
|
ABG's in Sarcoidosis?
|
Hypoxemia with Chronis hypocarbia (Low CO2)
|
|
|
Diagnosis of Sarcoidosis?
|
- Always consider with Bilateral Hilar adenopathy
- Liver Biopsy - may not be specific - **Mediastinoscopy** - Biopsy of Paratracheal nodes - Transbronchial Lung Biopsy |
|
|
Treatment of Sarcoidosis?
|
- Steroids - especially for extra-pulmonary involvement
- 40-60 mg prednisone daily - Not clearly shown to reverse or arrest progession of pulmonary involvement |
|
|
What is Pneumoconioses?
|
Occupational Lung Diseases
- Caused by the inhalation of inorganic dusts deposited in Distal bronchioles and alveoli - repeated exposure in most cases |
|
|
Three most common Pneumoconioses?
|
Silicosis
Asbestosis Anthracosis |
|
|
What is Silicosis caused by?
|
Silicon dioxide - quartz
- Sandblasting, mining -> glass, brick, tile, pottery, masonry, construction |
|
|
What is Asbestosis caused by?
|
Fireproofing, insulation, removal
|
|
|
What is Anthracosis caused by?
|
Coal, Black Lung, Coal Workers' Pneumoniocosis
|
|
|
What is Byssinosis caused by?
|
Cotton Dust
"Monday Fever" Brown Lung |
|
|
What is the presentations of occupational Lung disease?
|
- Gradual slow, progression, Chronic more than 20 years in some cases
- Most Preventable - Presentation variable with amount, length of exposure |
|
|
What is silicosis characterized by?
|
Unevenly distributed nodules in connective, small arterioles, alveolar walls
- Progressive - Massive fibrosis - Development of TB infection is common |
|
|
What does silicosis X-ray look like?
|
Classic - eggshell calcification highly suggestive
- Calcification on periphery of nodules |
|
|
What is Asbestosis?
|
Progressive Inflammation and Fibrosis
- Nonspecific more significant at lung bases - May be presence of Asbestos bodies in sputum --fiber coated by iron-protein complex |
|
|
What are different types of fibers?
|
Medically most damaging = crocidolite amosit
Aociation with crocidolite fibers - needle like (need little exposure) |
|
|
Association with lung cancer of occupational lung diseases?
|
25% of deaths
Smoking increases the risk to 90x more likely Mesothelioma |
|
|
What is Coal Worker's Pneumoconiosis?
|
Pathologic lesion
- Coal Macule more than or equal to 5 mm in diameter - Accumulation of macrophage that have ingested coal dust - Peribronchial regions - Results in deposition of reticulin, collagen fiber ->fibrosis |
|
|
What is Coal Workers Pneumoconiosis associated with?
|
Occupational Bronchitis
- Alveolar ducts dilated - centrilobar emphysema |
|
|
What is Allergic Alveolitis
|
Hypersensitivity pneumonitis
- Immunologically mediated disease caused by inhalaation of antigenic organic dusts (molds, fungal spores, animal proteins) - Infiltation of alveolar wall with PMN, eosinophils - Non-caseating granuloma - May progress to massive fibrosis |
|
|
Etiology of Allergic Alveolitis
|
Often occupational
- Farmer's Lung - Spores in the hay - Presentation often similar to asthma - Bronchopulmonary Aspergillosis |
|
|
Symptoms of Allergic Alveolitis
|
Dyspnea, Cough, Wheezes***
Fever, Chills Myalgia Anorexia Acute Symptoms resolve spontaneously (repeated bouts with exposures) Chronic Progressive Form: dyspnea |
|
|
Diagnosis of Allergic Alveolitis?
|
History of exposure to known antigen
Biopsy |
|
|
Pulmonary Function Test of Allergic Alveolitis?
|
Decrease diffusion, Restriction
Some Obstruction, reduced Airflow |
|
|
Treatment of Allergice Alveolitis?
|
Removal from Contact
Steroids in specific cases |
|
|
Pathogenicity of Drug Induced Lung Disease
|
Hypersensitivity pneumonitis
Direct Pulmonary Toxicity A-C Permeability - > Acute Pulmonary Edema Coma, Marked Respiratory Distress Rebound within 24 hours |
|
|
Intervention of Interstitial Lung Disease
|
Interstitial Lung disease has become more accurate as a result of thoracoscopy. (can be biopsed and scanned to determine the presence of this disorder without the need to a large incision)
|
|
|
Treatment for IPF
|
Standard treatment is to improve symptoms and slow progression of the disease
- Corticosteroids and cytotoxic drugs aim to reduce inflammatory reaction and preven the scarring and thickening of Lung tissues - Lung Transplantation has been successful as a treatment of LAST RESORT |
|
|
Three steps for Arteriole Blood Gas interpretation
|
1 - Is it acidosis or alkalosis
2 - what is the primary problem - Metabolic or respiratory 3 - Is there any compensation by the patien |
|
|
What are the normal values of the blood?
|
pH - 7.35 to 7.45
paCO2 - 36 to 44 mmHg HCO3 - 22-26 meq/L |
|
|
paCO2>44 with a pH<7.35 Represents
|
respiratory acidosis
|
|
|
paCO2<36 with a pH>7.45 Represents
|
Respiratory Alkalosis
|
|
|
For a primary respiratory problem pH and paCO2 move...
|
In opposite directions
- For each deviation in paCO2 of 10 mmHg in either directio, 0.08pH units change in the opposite direction |
|
|
HCO3<22 with a pH <7.35 Represents
|
Metabolic acidosis
|
|
|
HCO3>26 with a pH>7.45 Represents
|
Metabolic Alkalosis
|
|
|
For a primary metabolic problem pH and HCO3 move..
|
In the same direction and paCO2 is also in the same direction
|
|
|
What is compensation?
|
The Body's attempt to return the acid/base status to normal
|
|
|
Primary Problem - - - - Compensation
Respiratory Acidosis Respiratory Alkalosis Metabolic Acidosis Metabolic Alkalosis |
Metabolic Alkalosis
Metabolic Acidosis Respiratory Alkalosis Respiratory Acidosis |
|
|
What is the Expected compensation for respiratory Acidosis in the acute phase?
|
the pH decrease 0.08 units for every 10 mmHg increase in paCO2: HCO3 increase 0.1-1 mEq/liter per increase 10 mmHg paCO2
|
|
|
What is the expected compensation for respiratory acidosis in the chronic phase?
|
the pH decreases 0.03 units for every 10 mmHg increase in paCO2: HCO3 increase 1.1-3.5 mEq/liter per increase 10 mmHg paCO2
|
|
|
What is the expected compensation for respiratory alkalosis in the acute phase?
|
the pH increase 0.08 unites for ever 10 mmHg decrease in paCO2; HCO3 decrease 0-2 mEq/liter per decrease 10 mmHg paCO2
|
|
|
What is the expected compensation for respiratory alkalosis in the chronic phase?
|
the pH increase 0.17 units for every 10 mmHg decrease in paCO2; HCO3 decrease 2.1-5 mEq/liter per decrease 10 mmHg paCO2
|
|
|
What is the expected compensation for Metabolic acidosis?
|
paCO2 = 1.5(HCO3) + 8 (+_2)
paCO2 decreases 1-1.5 per 1 mEq/Liter HCO3 |
|
|
What is the expected compensation for Metabolic Alkalosis?
|
paCO2 = 0.7(HCO3) + 20 (+_1.5)
paCO2 increases 0.5-1.0 per increase 1 mEq/liter HCO3 |
|
|
what is seen in Acute Respiratory Acidosis?
|
paCO2 is elevated and pH is acidotic
the decrease in pH is accounted entirely by the increase in paCO2 - Bicarbonate and base excess will be in the normal range because the kidney's have not had adequate time to establish effective compensatory mechanism |
|
|
Causes of Acute Respiratory Acidosis?
|
- Respiratory pathophysiology - Airway obstruction, severe pneumonia, chest trauma/pneumothorax
- Acute drug intoxication (narcotics, sedatives) - Residual neuromuscular bloackade - CNS disease (head trauma) |
|
|
What is seen Chronic Respiratory Acidosis?
|
paCO2 is elevated with a pH in the acceptable range
- Renal mechanisms increase the excretion of H+ within 24 hours and may correct the resulting acidosis caused by chronic retention of CO2 to a certain extent |
|
|
What are the causes of Chronic Respiratory Acidosis?
|
- Chronic Lung Disease (BPD, COPD)
- Neuromuscular disease - Extreme obesity - Chest wall deformity |
|
|
What is seen in Acute Respiratory Alkalosis?
|
paCO2 is low and pH is alkalotic
- the increase in pH is accounted for entirely by the decrease in paCO2 - Bicarbonate and base excess will be in the normal range because the kidneys have not had sufficient time to establish effective compensatory mechanism |
|
|
Causes of Respiratory Alkalosis?
|
Pain, Anxiety, Hypoxemia, Restrictive lung disease, Severe Congestive Heart Failure, Pulmonary embolie, Drugs, Sepsis, Fever, Thyrotoxicosis, Pregnancy, Overaggressive mechanical ventilation, Hepatic Failure
|
|
|
What is Uncompensated Metabolic Acidosis
|
Normal paCO2, Low HCO3, and pH less than 7.30
- Occurs as a result of increased production of acids and/or failure to eliminate these acids - Respiratory system is not compensating by increasing alveolar ventilation (hyperventilation) |
|
|
What is compensated Metabolic Acidosis
|
paCO2 less than 30,
Low HCO3 with a pH of 7.3-7.4 |
|
|
Elevated AG Metabolic Acidosis causes?
|
- Ketoacidosis - Diabetic, alcoholic, Starvation
- Lactic acidosis - hypoxia, shock, sepsis, seizures - Toxic ingestion - methanol, ethylene glycol, ethanol, isopropyl alcohol, paraldehyde, tolune - Renal Failure - uremia |
|
|
Causes of Normal Anion Gap Metabolic Acidosis
|
Renal Tubular Acidosis, Post Respiratory Alkalosis, Hypoaldosteronism, Potassium sparing Diuretics, Pancreatic loss of bicarbonate, Diarrhea, Carbonic anhydrase inhibitors, Acid Admin, Sulfamylon, Cholestyramine, Ureteral diversion
|
|
|
Effectiveness of oxygenation in Hypoxemia
|
Decrease Oxygen content of blood - paO2 less than 60 mmHg and the saturation is less than 90%
|
|
|
Effectiveness of Oxygenation in hypoxia?
|
Inadequate amount of oxygen available to or used by tissues for metabolic needs
|
|
|
Mechanisms of hypoxemia
|
Inadequate inspiratory partial pressure of oxygen
Hypoventilation Right to left Shunt Ventilation-perfusion mismatch Incomplete diffusion equilibrium |
|
|
What does Pulmonary Function Test do?
|
Measures the volume and the rate of airflow in the lungs
the purpose is to diagnose and measure the severity of breathing problems |
|
|
Indications to do PFT's
|
- Preoperative Evaluations
- Evaluations of pulmonary symptoms - Assessment of treatment effectiveness - Monitoring disease progress - Screening for reactive airway disesase - Research |
|
|
What affects PFT's
|
- Gender
- Height - Age - Weight - Effort/Compliance/Cooperation - Race |
|
|
What is Spirometry?
|
most commonly ordered to evaluate air flow and lung volumes
|
|
|
What to tell the patient before a PFT
|
Eat a light meal
No Smoking for 4-6 hours Avoid taking certain medications (sedations) |
|
|
Criteria for acceptability in PFT's tests
|
- Lack of artifact
- Good Start of test without hesitation - Satisfactory exhalation with 6 second of smooth continuous exhalation - Plateau in the volume curve of 1 second |
|
|
Criteria for Reproducibility in PFT
|
Obtain 3 acceptable spirograms
|
|
|
Normal Lung Function in PFT
|
Very Few
- If your testing there is usually and should be an issue - All values 80% of predicted - Normally athletes |
|
|
Obstructive Lung Disease
|
- Patient with decreased expiratory airflow
- Volumes Normal to above-normal - Decrease FEV1/FVC ratio - FEV1 decreased - TLC increased - Decreased FEF25075 most sensitivie and first value to decrease |
|
|
What are some obstructive Lung Diseases
|
COPD
Emphysema Chronic Bronchitis, Asthma Cystic Fibrosis and Bronchiectasis Common Thread: Bronchoconstriction, inflammation, increased secretions, loss of lung elasticity or any combination |
|
|
What does Restrictive Lung diseases look like with PFTs
|
- Decreased lung volumes with normal airflow
- TLC decreased - FVC decreased or normal - FEV1 Normal or increased - RV/FRC decreased |
|
|
What are some restrictive lung diseases?
|
- Pleural Diseases
- Alveolar Diseases - Interstitial Diseases - Neuromuscular - Thoracic cage |
|
|
What is DLCO
|
Carbon Dioxide Dilution Capacity
|
|
|
DLCO
|
- is abnormal in most lung disease
- Increased is rarely important, occurs with polycythemia or lung hemorrhage - Asthma sometimes normal to increased - Emphysema decreased - alveoli working but the restrictive goes down - Obstructive low COPD |
|
|
What is Methacholine Provocation?
|
- Test that determines presence of airway hyperreactivity/reactive airway
- Spirometry done, Methacholine challenge give, Spirometry redone - Reduction of 20% below previous = Asthma - Reversed with Bronchodilator |
|
|
FEV1 tests results
|
- FEV1 <1 liter severe disease <50%
- FEV1 1-2 liters is moderate disease - 50-65% - FEV1 >2 liters mild disease 65-85% - Normal is >80% |
|
|
What is the definition of Acute Bronchitis
|
Inflammation of the mucosal lining of the tracheobronchial tree
|
|
|
What is Acute Bronchitis caused by?
|
- Airborne Irritants - Smoke air pollution
- Aspiration of irritants (sea water, gastric reflux) - Inhaled allergens - Infections -Bacterial, Viral, Unresolved colds |
|
|
What does the clinical picture of acute bronchitis look like?
|
Varies upon severity and extent of process
- Can be mild with non-productive cough or severe to a point of suffocation - Auscultation - Rales, Rhonchi, and expiratory wheeze - Mild Fever - Increase WBC |
|
|
What is the hallmark of obstructive Disease?
|
Expiratory wheezes
|
|
|
What are the types of cough with Acute Bronchitis?
|
- May be non-productive or productive
--mucoid, mucopurulent or purulent - Paroxysmsmal - brought on by change in position, cold temperature, exertion, smoking, talking, laughing |
|
|
Progression of Acute Bronchitis?
|
- Usually starts 1-2 days as upper respiratory infection, and gradual onset of cough
- Followed by wheezing, acute respiratory distress (hyperinflation of lungs) - Usually lasts 7-10 days - Cough may last 6-8 weeks |
|
|
Treatment for Acute Bronchitis
|
- Bedrest
- Antibiotics if bacterial - Fluids - High Humidity - Bronchodilator if needed - Steroids for inflammation, unresolved cough - Anti-tussive agents of non-productive |
|
|
What is the definition of Chronic Bronchitis?
|
A chronic productive cough without other demonstrable cause
- **Expectoration most days for 3-4 more consecutive months for 2 successive years - 90% are smokers - Pollution is a factor |
|
|
Symptoms of Chronic Bronchitis?
|
- Productive morning cough
- Frequent attacks of acute bronchitis in cold weather - Dyspnea usually not marked unless CHF intervenes - Wheezes, Diminished breath sounds - Slow progressive onset over many years |
|
|
Physical Findings of Chronic Bronchitis?
|
Later in the disease
- Normal to Barrel Chest - Cyanosis - Blue Bloaters - Hypoxia, Hypercapnea (extra CO2) - 2nd polycythemia (excessive RBC) - Use of accessory muscles - Percussion note - Hyperresonant |
|
|
What is Cor Pulmonale?
|
- Seen in Right heart Failure - Peripheral edema, JVD, Hepatomegaly
- P-2 accentuated - Right axis deviation (Downward deflection of QRS in Lead 1, Large Peaked P waves) - Right Ventricular Heave - (Pounding against left sternal border on PE) |
|
|
Pathologic Changed in Chronic Bronchitis?
|
- MCE thickened, inflammed - Swelling and hypertrophy
- Increase mucous production - thick tenacious, increase goblet cells, submucosal glands - decrease in number of cilia - Broncho spasm |
|
|
What does the sputum look like in Chronic bronchitis?
|
Mucoid unless chronic infections then turn mucopurulent
|
|
|
Most common organisms in Sputum of Chronic Bronchitis?
|
Hemophilus Influenza
Streptococcus Moraxella - second |
|
|
X-ray of Chronic Bronchitis?
|
Early - Change not significant
Late - Hyperinflation with flattened Diaphragm Pulmonary hypertension (enlarged heart) - Increased Vascular markings at bases |
|
|
PFT's in Chronic Bronchitis
|
Early - May be normal, except for slight decrease in expiratory flow rates
Progression: - Decrease Flow rates - **Normal to Decreased VC, Increased FRC, RV - Normal Elastic recoil diffusing capacities |
|
|
Treatment of Chronic Bronchitis
|
Slow Progression, Treat Complications
- Stop Smoking - Hydration - Avoid Irritants - Anything that will compromise the airway - Bronchodilator therapy - to expand the airway - Steroids - Antibiotics when specific pathogens are noted |
|
|
Pulmonary Rehab with Chronic Bronchitis
|
Goal to increase ADL
PFT may not improve - need to make sure to keep O2 and CO2 levels at good levels to keep the drive to breath there |
|
|
Emphysema definition
|
- Anatomical alteration of lung
- Characterized by abnormal enlargement of air spaces, distal to terminal, non-respiratory bronchiole, accompanied by destructive changes of alveolar walls |
|
|
Compensatory Emphysema
|
Non-obstructive pulmonary over-inflation
- Simplest Form - Produced when a portion of the lung removed, remainder fills with space - Atelectatic (obstruction, scarring) - remaining segments overdistended |
|
|
Localized Overinflation
|
Localized obstructive emphysema
Partial obstruction of Bronchus (foreign body or tumor, |
|
|
Senile Emphysema
|
- Barrel Chest with Aging
- Kyphotic spinal changes enlarge alveoli - minimal sequelae - Associated with reduced PaO2 |
|
|
Subcutaneous, Mediastinal Emphysema
|
- "Rice Krispies", Crepitus
- Presence of air in subcutaneous tissue over thorax, neck and face ==usually from bronchial injury, air travels from mediastinum ==Often sign that mediastinal emphysema pneumothorax present |
|
|
Pulmonary Emphysema
|
Chronic COPD
Non reversible and progressive |
|
|
What is Pulmonary Emphysema characterized by?
|
- Hyperinflation
- Loss of Elastic Recoil (increase Clt) - Increase FRC, RV, TLC (Barrel Chest) - Airway obstruction =Mechanical in nature = Decrease airflow in small airways |
|
|
Impaired O2 diffusion with Emphysema
|
- Loss of Surface area for gas exchange
- Capillaries destroyed along with Septa - Degenerative, perivascular changes -> increased PVR ->Cor Pulmonale |
|
|
Classifications of Emphysema
|
Bullous
Centrilobular Panlobular Alpha-antiprotease deficiency Mixed |
|
|
What is Bullous Emphysema
|
Not separate entity
- Thing walled multiple cysts = Bulla = >1 cm = Bleb = superficial subpleural = Cyst = Large = Pneumatoceles = huge - Pneumothorax |
|
|
Centrilobular (Centriacinar) Emphysema
|
- Most Common - Overlap with Chronic Bronchitis
- Associated with Smoking, Coal Miners, Pneumoconiosis - Major problem with respiratory bronchioles - Often localized in Apices |
|
|
What is a Blue Bloater
|
- Typical COPD
- Retain CO2 - hypoxic Drive - Cannot be detected clinically or radiologically until advanced |
|
|
Panlobular
|
- Pure Emphysema
- Less common, involves entire acinus, alveoli not respiratory bronchioles - Ventilation, perfustion and diffusion involved |
|
|
What is a Pink Puffer?
|
Do No retain CO2 until end stage
- Advanced COPD - Intense Dyspnea - Marked Weight Loss - Small Heart |
|
|
Etiology of Alpha-1 Antiprotease Deficiency
|
- Not common only 1-2% of cases
- Usually occurs age 30-40, non-smokers - Genetic heredity |
|
|
What is Alpha Antitrypsin
|
- Enzyme normally prevents proteases from digesting lung tissue
= Component of Normal Adult globulin = Protease in lymphocytes, macrophage, break down alveolar walls - New Drug - Prolasting for Treatment |
|
|
What are Clinical Signs and Symptoms of Alpha-1 Antiprotease Deficiency
|
1. Accessory Muscle Use, 2. Pursed-lip breathing, 3. Dyspnea, 4. Rhonchi, wheezes, dimished, 5. Barrel Chest, 6. Prolonged expiration, 7. Fatigability, weight loss, anorexia, 8. Emotional component of dyspnea very strong: Fear, apprehension, depression
|
|
|
PFT's in Alpa-1 Antiprotease deficiency
|
- Minimal Bronchodilator response
- Increased FRC, RV - Decreased Diffusing Capacity *** |
|
|
X-ray in Alpha-1 Antiprotease deficiency
|
- Flattening of Hemi-diaphragms, presence of bullae
- Hyperlucent, increased AP diameter, Horizontal ribs - Decreased vascular markings, especially at apices |
|
|
Functional Classification of Emphysema
|
Grade 1: Can keep pace walking with persons of same age and bosy build on the level of breathlessness, but not on hills or stairs
Grade 2: Can walk a mile at own pace, Dyspnea, but cannot keep pace on the level with a normal person Grade 3: Becomes breathless after walking about 100 yards or for a few minutes on a level Grade 4: Become breatheless while dressing or talking |
|
|
Treatment of Emphysema
|
Geared to Bronchitic Component, Nasal oxygen,
Adequate hydration, nutrition, bronchial hygiene, Bronchodilators, Xanthines, May use steroids, Antibiotics, Diuretics, Inotropic agents, anti-arrhythmics for cardiace complications, Anticoagulants |
|
|
Goals of Pulmonary Rehab
|
- Exercise training, education, psychosocial
- Increased ADL, patients "Feel" better - Does nor improve PFT by number - Decrease hospitalizations and therefore cost effective |
|
|
What is Acute Respiratory Failure
|
Associated diffuse pulmonary injury presenting with marked respiratory distress and hypoxemia
- Final common pathway of acute diffuse lung injury from variety of causes |
|
|
Etiology of Acute Respiratory Failure
|
Acute Restrictive Disease of Diminishing FRC
- Lack of surfactant or abnormal function - Symptoms very similar to infant RDS |
|
|
Acute Respiratory Failure Can occur following:
|
Shock, Thoracic Trauma, Pulmonary Contusion, Aspiration, Sepsis, O2 Toxicity, Extensive Burns, Fat Embolism, Large Transfusion, Acute Pancreatitis, Narcotic Drug OD, DIC (disseminated INtravascular coagulation, Near Drowning, Radiation
|
|
|
Pathogenesis of Acute Respiratory Failure
|
Exact Mechanism of acute lung injury not known
Microembolus formation of WBC, Platelets, Fibrin, neutrophils with enzymatic and toxic products Immunological reactions, release of vasoactive chemical mediators |
|
|
Physiologt of Fluid movement in Acute Respiratory Failure
|
in Alveolar interstitium
- ARDS disturbance of normal barrier limiting leakage of fluid out of pulmonary capollaries and into parenchyma |
|
|
Definition of Pneumonia
|
Infection of the alveoli, distal airways and the interstitium of the lungs as manifested by increased weight and consolidation in the lungs.
|
|
|
Classification of pneumonia
|
Community Acquired Pneumonia
Nosocomial |
|
|
Pathogenesis of Pneumonia depends on?
|
- Size of the inoculum
- Virulence of the organism - Condition of the host |
|
|
What are the defenses against Pathogenesis?
|
- Upper Airway - first line
- Glottis is the next time of defense - Lower Airway defenses - (Alveolar Macrophages, Surfactant, IgG, Complement and other factors that kill and process foreign proteins like bacteria and viruses, Macrophage response is T-cell mediated, Epithelial cells produce antimicrobial molecules and recruit polymorphonuclear leukocytes) |
|
|
Methods of Inoculation for pneumonia
|
- Inhalation of infected aerosols
- Aspiration of oropharyngeal secretions - Hematogenous spread |
|
|
Signs of Pneumonia
|
- Fever or Hypothermia
- Sweats - Chills - Fatigue - Myalgias - Headache - Abominal Pain - Chest Discomfort - Cough (productive or nonproductive) |
|
|
Symptoms of Pneumonia
|
- Hemoptysis
- Dyspnea - Elderly with confusion - Tachypnea - Tachycardia - Adventitious Breath sounds and/or diminished breath sounds - Dullness to percussion |
|
|
What is the most common cause of Community Acquired Pneumonia?
|
S. Pneumonia
|
|
|
How to Diagnose Community Acquired Pneumonia?
|
- History and Physical
- Chest X-ray - helpful only if infiltrate present and not pathognomonic for type of pneumonia - Definitive ID by: Direct culture of sputum, Analysis of blood, pleural fluid, lung tissue, Urine Antigen (Legionella Pneumonia and Strep Pneumonia) |
|
|
How to asses Mortality Risk for Community Acquired Pneumonia
|
- Advanced Age
- Alcoholism - Comorbid medical conditions - Altered Mental Status - Respiratory Rate >30 b/min - Hypotension - BUN >30 mg/dL |
|
|
Causative Organisms for Community Acquired Pneumonia
|
Step. Pneumonia
Hemophilus Influenza Staph. aureus Moraxella catarrhalis |
|
|
Atypical Causative Organism for Community Acquired Pneumonia
|
Mycoplasm
Clamydia Legionella |
|
|
Causative Organisms in Viral Pneumonia
|
Influenza
RSV Adenoviruses Parainfluenza Coronavirus (SARS) |
|
|
Strep. pneumonia Community Aquired Pneumonia, basic facts
|
Most common pathogens
Gram positive diplococci Common in patients with coexisting cardiopulmonary disease |
|
|
Signs and symptoms of Strep pneumonia
|
Fever, Chills, Productive cough
|
|
|
Treatment for Strep. pneumonia
|
Penicillin G
Amoxicillin Macrolides Fluoroquinolones Cephalosporins Clindamycin Vancomycin |
|
|
Prevention of Strep pneumoniae
|
Polyvalent pneumococcal vaccination
|
|
|
Hemophilus Influenza - Community Acquired Pneumonia - basic facts
|
Gram Negative coccobacilli
Follows URI and common in patients with coexisting cardiopulomonary disease Common in smokers |
|
|
Complications of Hemophilus influenza - Community Acquired Influenza
|
Endocarditis and emphysema
|
|
|
Treatment of Hemophilus Influenza
|
Cephalosporins
Macrolides Bactrim Second line - Fluoroquinolones |
|
|
Staph Aureus - Community Acquired Pneumonia general comments
|
Gram Positive
Consider during Influenza epidemics Must Rule out MRSA |
|
|
Who do you consider Staph aureus in what patients
|
- In Chronic care communities
- Cystic fibrosis patients - Patients with bronchial disease - IV drug users |
|
|
Treatment of Staph aureus
|
If no MRSA:
- Augmentin - Cephalosporins with out without rifampin or gentamycin If MRSA: - Gentamycin - Rifampon |
|
|
General Statements about Moraxella catarrhalis in Community Acquired Pneumonia
|
- Gram negative diplococci
- Consider during influenza epidemics - Must rule out MRSA |
|
|
Who to consider Moraxella catarrhalis to have it?
|
Patients with pre-existing lung disease and those on immunosupressive therapy
|
|
|
Treatment of Moraxella catarrhalis
|
- Augmentin
- Bactrim - 2nd or 3rd generation cephalosporins - Second line - fluoroquinolones |
|
|
Mycoplasma Pneumonia general Statements:
|
- Most common in young adults
- Etiology: Mycoplasma pneumoniae - Peaks in fall |
|
|
How may mycoplasma pneumonia present?
|
- Rash
- Fatigue - Nonproductive cough - Nonexudative pharyngitis - Myalgias - Lymphadenopathy - splenomegaly - conjuctivitis |
|
|
Treatment of Mycoplasma pneumonia
|
- Macrolides
- Doxycycline - Erythromycin |
|
|
Etiology of Legionella Pneumonia
|
Fastidious gram negative bacillus, Legionella pneumophila, distributed in water delivery systems
|
|
|
Signs and symptoms of Legionella Pneumonia
|
Dry cough, Respiratory Distress, Fever, Rigors, Malaise, weakness, headache, confusion, GI disturbances
|
|
|
How do you diagnose Legionella Pneumonia
|
- Direct immunofluoresence test
- Legionella antigent in urin 70% of cases |
|
|
Treatment of Legionella Pneumonia
|
Macrolides
Doxycycline Rifampin may be added |
|
|
Etiology of Viral Pneumonias
|
- Influenza
- RSV (Most common in young children) - Adenoviruses - Parainfluenza - Coronavirus (SARS) |
|
|
Treatment of Viral Pneumonia
|
- Supportive Care
- Severe cases may require admissions, treatment with antivirals and macrolides, hydration and suction |
|
|
Aspiration Pneumonias facts
|
- Accounts for 49% of hospitalization for pneumonia
- Must ID aspirate (most likely gastric) |
|
|
Etiology of Aspiration Pneumonias
|
Chemical from gastric contents
- Bacterial =Klebsiella pneumonia = pseudomonas influenza |
|
|
Treatment of Aspiration Pneumonia
|
- Supportive Care
- Antibiotic depending on culture - often hospital vancomycin is necessary - Watch for ARDS - mortality as high as 23% |
|
|
Etiology of Pneumocystis Pneumonia
|
Fungal Organism - Pneumocystis jiroveci
- Most common opportunistic infection in HIV+ |
|
|
Diagnosis of Pneumocystis Pneumonia
|
- Diffuse bilateral infilitrates extending from the perihilar region are seen in most patients
- Sputum for PCP cyst - Bronchoscopy if Sputum undignostic - LDH usually elevated - NOT Specific |
|
|
Treatment of Pneumocystis Pneumonia
|
- Bactrim
- Dapsone - May add prednisone if arterial O2 is <70% |
|
|
Causes of Exposure Pneumonias
|
- Cattle Sheep: Brucellosis, Q Fever
- Rabbits: Tularemia - Birds, Bats: Psittacosis, Histoplasmosis - Rodents: Hantavirus - Dog Ticks: Erlichiosis - SW US: Coccidiomycosis (Valley Fever) - Developing Countries: TB |
|
|
Definition of Nosocomial Pneumonia
|
Pneumonia that occurs more than 48 hours after admissions to the hospital and excludes a pre-existing diagnosis of pneumonia
|
|
|
Diagnosis of Nosocomial Pneumonia?
|
At least of 2 of the following:
- Fever - Cough - Leukocytosis - Purulent sputum New or progressive parenchymal infiltrate on CXR |
|
|
What do you have to rule out with nosocomial pneumonia
|
- Pulmonary emboli
- Cardiac Failure - Atelectasis - ARDS - Drug Reactions - Pulmonary Hemorrhages |
|
|
Nosocomial Pneumonia work up
|
- Sputum Colutes
- Pulse oximetry and/or ABG - CXR - Tap Pulmonary effusions |
|
|
Etiology of Nosocomial Pneumonia
|
Pseudomonas aeroginosa - Gram negative rods
- May Cause cavitation on radiography Klebsiella psumoniae and E. coli. - Gram negative - Seen in Chronic alcoholics and diabetics |
|
|
Who is most susceptible in Nosocomial Pneumonia
|
ICU and Ventilation Patient
|
|
|
Treatment of Nosocomial Pneumonia
|
- Initiate as soon as possible
- Vancomycin is MRSA suspected |
|
|
Treatment of Patients without risk factors for nosocomial pneumonia
|
- 2nd generation cephalosporin
- Nonantipseudomonal 3rd generation cephalosporin - Combination or beta lactam and beta lactamase inhibitor |
|
|
Treatment for late onset or ventilator associated Nosocomial Pneumonia
|
- Combination of antibiotics against the most virulent organism
- Aminoglycoside or fluoroquinolone PLUS - Antipseudomonial penicillin or cephalosporin - May use carbapenem or aztreonam |
|
|
How do you treat pneumonia in Immunocompromised Host
|
- Sputum analysis
- if nondiagnostic, bronchoscopy, transthoracic needle biopsy, or open lung biopsy |
|
|
Forced Vital Capacity
|
Forced expiration in the spiromrey
Inspire fully and expires all the air lungs as fast as he can |
|
|
A patient with an obstruction of Upper Airway has ______ FEV1
|
Diminished
|
|
|
A patient with restriction of the pulmonary volume has a _____ FEV1
|
too high
|
|
|
Peak Flow
|
Measure for the air expired from the large upper airways (Trachea-bronchi)
|
|
|
Restrictive Lung disease mean the lung volume is
|
to low
|
|
|
a Patient with obstructive lung disease typically has a ________ F/V loop
|
Concave
|
|
|
COPD
|
heterogeneous disorder that includes emphysema, chronic bronchitis, obliterative bronchitis, and asthmatic bronchitis
|
|
|
GOLD guidelines of COPD
|
a disease state characterized by airflow limitation that is not fully reversible
|
|
|
Airflow in COPD
|
usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases
|
|
|
ATS/ERS definition of COPD
|
A Preventable and treatable disease state and adds that the noxious particles or gases are primarily caused by cigarette smoking
|
|
|
Chronic Bronchitis Definition
|
Defined clinically as chronic productive cough on most days for 3 months in each of 2 consecutive years in a patient in whom other causes of chronic sputum production have been excluded
|
|
|
Definition of Emphysema
|
defined pathologically as the presence of abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis
|
|
|
What should COPD patients with intermittent symptoms receive
|
short acting bronchodilator
|
|
|
What should Stage 3 COPD patients with frequent exacerbations
|
inhaled corticosteroids should be part of their regular therapy
|
|
|
what is the most important risk factors in COPD
|
Smoking leads to an inflammatory response, oxidative stress, lung destruction and interference with lung repair
|
|
|
Host factors for COPD
|
Genetic factors
Airway hyper responsiveness Lung Growth |
|
|
Risk Factors for COPD with exposures
|
- Tobacco Smoke
- Occupation dusts and chemicals - Indoor and outdoor pollution - Broncho - Pulmonary infections - Socioeconomic status |
|
|
Pathology and Pathogenesis of COPD
|
Pathologic changes in the central airways, peripheral airways, lung parenchyma, and pulmonary vasculature, changes which are variably present in affect patients
|
|
|
Anatomic Changes with COPD
|
- Changes in Bronchi
- Chronic hypersecretion of mucous changes in central airways - Bronchial Gland hypertrophy and goblet cell metaplasia result from smoking - Smokers - goblet cells are more numerous and extend peripherally |
|
|
Anatomic Changes in Emphysemia
|
loss of attachements and loss of elasticity, which contributes to small airways collapse during expiration via loss of tethering effect
|
|
|
Two major types of Emphysema according to the distribution within the acinus
|
1. Centrilobar emphysema - involves dilation of the respiratory bronchioles, type seen in smokers
2. Panlobular emphysema which involved destruction of the whole acinus and which occurs with alpha1-antitrypsin deficiency |
|
|
Bullae
|
Localized areas of emphysema that have over distended and are classified by their size and position
|
|
|
Blue Bloater - Anatomic Changes
|
phenotype with swollen ankles, enlarged liver, and engorged neck veins occurs in end-stage COPD dur to remodeling of the pulmonary arteries as a result of alveolar hypoxia
- Early changes are thickening of the intima, increase in smooth muscle and infiltration of inflammatory cells into the vascular wall. - Later - RV hypertrophy and 2ndary pulmonary hypertension develop in patients with chronic hypoxemia - Vascular changes can be aggravated by coexistent Obstructive sleep apnea |
|
|
Key to diagnosis of COPD
|
expiratory airflow limitation
|
|
|
Classification of Severity of Chronic Obstructive Pulmonary disease
Stage 0 |
Normal Spirometry
Chronic Symptoms (Cough sputum production) |
|
|
Classification of Severity of Chronic Obstructive Pulmonary disease
Stage I: Mild |
FEV1/FVC <70%
FEV1 >_ 80% predicted with or without chronic symptoms (cough, sputum production) |
|
|
Classification of Severity of Chronic Obstructive Pulmonary disease
Stage II: Moderate |
FEV1/FVC <70%
50% <_ FEV1 <80% predicted with or without chronic symptoms (Cough, sputum production) |
|
|
Classification of Severity of Chronic Obstructive Pulmonary disease
Stage III: Severe |
FEV1/FVC <70%
30% <_FEV1 <50% predicted with or without chronic symptoms (Cough, sputum production) |
|
|
Classification of Severity of Chronic Obstructive Pulmonary disease
Stage IV: Very Severe |
FEV1/FVC <70%
FEV1 < 30% predicted or FEV1<50% Predicted plus chronic respiratory failure |
|
|
What is given in early-state COPD?
Management |
Short-acting B2-agonist or anticholinergic bronchodilartoes are given as needed but as the disease progresses, they are given regularly to relieve symptoms and improve exercise tolerance
|
|
|
4 components of COPD management by GOLD standards
|
assess and monitor the disease
Reduce the risk factors manage stable COPD Manage exacerbations |
|
|
Goals of management of COPD
|
Prevent progression
Relive symptoms improve exercise tolerance improve health status prevent and treat complications prevent and treat exacerbations and reduce mortaility |
|
|
Corticosteroids in COPD
|
COPD is corticosteroid-insensitive and inhaled corticosteroids no not change the rate of FEV1 decline in affected patients
|
|
|
how is asthma characterized
|
by intermittent cough, shortness of breath, chest tightness andwheezing
|
|
|
Airway Remodeling
|
Structural alterations occur in the lungs of patients with asthma consisting of sub epithelial fibrosis, increased smooth muscle mass, angiogensis and hyperplasia of mucous gland and goblet cells
|
|
|
Chronic Stable COPD Treatment
|
- Patient and Family education
- Pharmacotherapy = Bronchodilators = Steroids (inhaled/oral) - Oxygen - Pulmonary Rehabilition - Surgery |
|
|
Three types of Bronchodilators in COPD
|
- Anticholinergics (inhaled)
- Beta-2-agonists - Methylxanthines |
|
|
Short acting Bronchodilators
|
- Improve Pulmonary Function/SOB/exercise performance
- Do Not affect QOL - Combination SABD's (beta-agonist and anticholinergics) produce a better bronchodilations - For patients with MILD symptoms - SOB on Exertion |
|
|
Long Acting Bronchodiolators
|
- For patients who still have symptoms on SABD's (Moderate disease)
- More sustained effect on PFT's, Chronic SOB and QOL - Anticholinergic - Tiotropium (OD) - Beta-2-agonists - Fomoterol, Salmeterol - Early evidence these may prolong time between exacerbations |
|
|
Bronchodilatos - Moderate -> Severe COPD
|
tiotropium
LABD SABD If still severe - may benefit from theophylline |
|
|
Steroids in COPD
|
- Inhaled and oral
- NOT recommended at first line therapy - No consistent effect on decreasing inflammation - Consider inhaled form in those with mod-severe disease - Consider in those who have MAXIMAL bronchodilator |
|
|
Patients who use Oral Steroids are at high risk for
|
- Cararacts
- Muscle Weakness - Hypertension - Osteoporosis - Diabetes |
|
|
Oxygen in COPD
|
- Definite Survival benefit in severe COPD
- Should be considered in patients with 1. Severe hypoxemia (PaO2 <55mmhg) 2. PaO2 <60mmHg + bilateral ankle edema, cor pulmonale |
|
|
Pulmonary rehabilitation with COPD
|
- they are deconditioned
- Leads to muscle wasting = dyspnea - |
|
|
Prevention in Chronic Exacerbation of COPD
|
- Flu Shot
- Pneumovax |
|
|
Acute Exacerbations
|
Sustained worsening of dyspnea, cough or sputum production leading to an increase in the maintenance medications and/or supplementation with additional medications
- Most common cause of administrations, ER visits and death in COPDers |
|
|
What do you with people who are having Acute Exacerbations of COPD
|
- CXR - need to rule out CHF, pneumonia and pneumothorax
- Spirometry - not useful in acute setting - ABG can be useful - Fever is uncommon |
|
|
Management of Acute Exacerbations in COPD
|
- Oxygen
- Bronchodilators - Steroids - Antibiotics - Non-invasive PPV |
|
|
Oxygen use in Acute Exaccerbation in COPD
|
- Excess use should be avoided
- However should not be withheld for hear of hypercapnea - O2 to maintain PaO2 at approx 60 mmHg - |
|
|
Bronchodilators in Acute exacerbation in COPD
|
- No difference in Beta-2-agonists and anticholinergics
- some benefit from combination - Don't start theophylline and don't use long acting agents |
|
|
Steroid use in Acute exacerbation of COPD
|
- Faster recovery and shorter hospitalizations
- May prolong time till next relapse - 5-14 days recommended - could have health consequences in short uses |
|
|
Antibiotics in Acute exacerbation of COPD
|
- Approx 50% exacerbation due to infectious etiology
- Mostly Bacterial - Especially helpful in severe exacerbation - Purulent Sputum more likely to benefit - Antibiotic resistance is an issue |
|
|
Common bugs in COPD patients Acute Exacerbation
|
Mild to Moderate: Strep. pneumonia, Haemophilus Influenza, Moraxella catarrhalis, Mycoplasma pneumonia, virus
Severe Exacerbation: Pseudomonas sp. gm-ve enteric bacilli |
|
|
Non Invasive Positive Pressure Ventilation
|
- Persistent acidosis despite adequate bronchodilators
- Decrease morbidity/mortality - Decrease the need to intubation/ventilation - Decrease length of ICU stay - Requires awake/alert/cooperative/hemo stable patient - if no improvement in 4 hours unlikely to benefit |
|
|
When to refer COPD Acute Exacerbation to a Specialist
|
- Diagnosis uncertain
- Symptoms are severe - Symptoms do not correlate with PFT's - Early onset - Accelerated loss of function (FEV1 decline >80ml/year over 2-year period) - Consideration for surgery |
|
|
Reasons for dramatic upswing of TB cases in US since 1984
|
HIV epidemic
Deterioration of the healthcare infrastructure program funding fell dramatically in the 80's increased number of cases amount 3rd world immigrants homelessness, poverty widespread drug abuse globilization |
|
|
Two types of TB
|
- Bovine type - rare in US
- M. avian seen in HIV (MAC) serious |
|
|
Characteristics of TB bug
|
- Sunglight, heat, phenol etc destroy the bacillus (resistant to acids, alkalis, antibacterial agents such as penicillin
- Can remain viable in dried sputum extensive periods of time viability related to concentration of chemical; time of exposure to physical and chemical agents |
|
|
Source of TB infection
|
1. Principle source - infected persons from respiratory secretion
2. Contaminated hands 3. Drinking infected cow milk 4. Ventilation systems with airflow of contaminated secretions 5. Once in the body it is transmitted by blood or lymph or in immunocompromised antigen-specific T cells activate macrophages 6. Can heal spontaneous 7. Transmission depends upon variables (infectivity of the source, immune defenses of the exposed, HIV) 8. Reactivation of old lesions 9. Not Highly infectious 10. Corticosteroids and immunosuppressants reactivate |
|
|
Why is TB not highly infectious
|
infection usually after long and close case exposure
- after infection progress depends on: 1. Number and virulence of the bacillus 2. Genetic mutation in the strain with drug resistance achievement 3. native and acquired resistance of the host including health of the immune system 4. hypersensitivity of the host (racial, women in early adulthood, age) |
|
|
Risk factors for TB
|
HIV, Age, Alcoholism and IV drug users, immunosuppression, silicosis, poor nutrition, diabetes, renal dialysis, organ transplant, previous residence in Asia, Africa or Latin America, High risk institutional settings (homeless shelters, correctional facilities)
|
|
|
Clinical Characteristics of TB
|
1. Usually have exposure history
2. From infection to positive skin test can be 3-8 weeks 3. Patients with pulmonary TB have systemic and pulmonary complaint (fever, chills, night sweats, anorexia, weight loss and fatigue, lower respiratory disease, cardinal respiratory symptom is chronic productive cough lasting over 3 weeks) 4. Physical findings initially are usually minimal (chest may have rales, signs of consolidayion, pleural effusion) |
|
|
How to Diagnose TB
|
1. TB skin test
2. Bacteriologic testing 3. Susceptibility testins 4. Radiography |
|
|
TB skin testing
|
- Positive 2-10 weeks after infection
- negative doesn't exclude the disease - sizes: 1.5cm for normal people 5 mm for people who are immunocompromised - Change from negative to positive usually means intervening infection - TB positive for 1 year without infection - good prognosis, reflects strong immune response, |
|
|
Bacteriologic testing of TB
|
- No organism in the sputum is a rough guide to infectivity
- Direct examination with Ziehl-Neelson Stain - 20% of patients with positive culture but negative smears - minimum 3 sputum specimen for culture on 3 days - 4-6 weeks to grow - PCR will ID small numbers bacteria in tissues |
|
|
Susceptibility testing of TB
|
- Must be performed on first isolate
- in 3 months in cultures still positive: 4 months: 6 months - Clinical evidence of failure to respond - DNA probing can eliminate M. avium in 1 day - Same Rapid-growth detection can be used for susceptibility - 1 week |
|
|
Radiography of TB
|
- Reactivated TB have apical disease with/without caviations
- May present as (adenopathy, infiltrate, caviation, pleural effusion, miliary pattern, single solitary nodule) - Appearance is not pathognomonic - Film is subjectibe - There is evidence that excellent TBC programs can be carried out without recourse to chest radiography |
|
|
Diagnosis of TB is made by:
|
- Assessing patients risk factors for infection
- Evaluating disease progression - Clinical features of the disease |
|
|
TB Pleural effusion
|
- fluid in the pleural space
- tap fluid and see what bugs are |
|
|
Extrapulmonary TB
|
- TB pleural effusions
- TB lymphadenitis - Spinal TB - Renal TB - Miliary TB - TB Meningitis |
|
|
TB lymphadenitis
|
scrofula
- Enlarged Lymph Nodes |
|
|
Spinal TB
|
- Can occur in any joint area
- TB of bone - Complain of bone pain and do X-ray and see degradation of bone |
|
|
Renal TB
|
- Pus in urine and blood in urine
- TB won't be affected by usual organisms |
|
|
TB meningitis
|
- Smear of SF usually negative but it needs to be cultured
- Have typical signs and symptoms of meningitis - head, neck and pain movement |
|
|
Methods for achieving goals of prompt evaluation and diagnosis for patients with suspected TB
|
Prompt Evaluation
- Chest X-ray - 3 or more sputum specimen with appropriate isolation precautions - body fluids and tissues biopsy as indicated Follow Up evaluation - Recognize when TB ruled out and stop therapy - Recognize clinical, culture negative TB requiring treatment - Recognize potential false-nagative TB cultures - Distinguish between true and false positive cultures for non-TB mycoblast |
|
|
Treatment of TB
|
Multidrug therapy to prevent failure during treatment and acquired response
- Four Drug regimen is preferred - Direct Observed Therapy |
|
|
Four Drug Therapy of TB
|
Isoniazid, Rifampin, Pyrazinaminde and Streptomycin or ethambutol
|
|
|
Management of TB in Immunocompromised patients
|
1. immunodepression causes rapid progress and death
2. Therapy usually needed for 18-24 months 3. If susceptibility tests not available treat with ethambutol or SM whole course to INH and Rifabutin |
|
|
Management of TB in Infants and children
|
treatment vigorous and soon as possible
|
|
|
Treatment of TB in pregnancy
|
- SM causes congenital deafness
- PZA questionable because risk of tatragenecity has not been determined - Preferred initial is INH, RIF,and EMB |
|
|
Isoniazid
|
- Most active Anti-TB dug.
- Bacteriocidal - Inexpensive - No Cross resistance between INH and other drugs - Well Absorbed from the gut and diffuses into all tissues including CNS - some resistance when used on its own - Used in active disease with Rifampin |
|
|
Toxic Reactions of Isoniazid
|
Insomnia and restlessness
fever and myalgia convulsions and psychotic episodes Peripheral neuritis liver problems |
|
|
Ethambutol
|
- only bacterionstatic first line
- well absorbed in the gut - Resistance is rapid when used alone - used as initial part of the 4 drugs |
|
|
Side effects of Ethambutol
|
Dose related optic neuritis
reduced acuity: problem with red-green discrimination, retinal damage at low doses side effects are rare |
|
|
Rifampin
|
1. Inhibits in vitro gram positive cocci, meningococci and TB
2. Penetrates into phagocytes and kills intracellulary 3. well absorbed and distributed 4. Excretes through the liver and less in urine 5. can have orange color to sweat urin and contact lens |
|
|
Adverse Effect of Rifampin
|
Rash and thrombocytopenia
Impaired liver and immune response increases metabolism of oral anticoagulants, oral antihyperglycemics, digoxin, steroids -*****Contraindicated in patients taking protease inhibitors and non-nucleoside reverse transcriptase therefore it is contraindicated in AIDS. use Rifabutin instead at half dose since metabolism is slowed by these drugs |
|
|
Streptomycin
|
1. Bacteriocidal in an alkaline environment
2. easiy resistant must use in combination 3. doesn't go into the CNS easily functions extracellularly 4. Can be renal toxix |
|
|
Pyrazinamide
|
1. Bacteriocidal in acid environment
2. Well absorbed and distributed - metabolized by kidneys 3. Can cause hepatitis |
|
|
Adverse effects of Pyrazinamide
|
Hepatotoxicity
Safety during pregnancy not established nausea vomiting drug fever hyperuricemia |
|
|
General Prevention and Control TB
|
1. Substandard housing replacement
2. Institutions and Hospital (control ventilation) 3. don't start preventative care until active disease is ruled out |
|
|
Categories for Preventive Chemotherapy
|
- Household members, close to recently persons
- Children especially until status is known - Skin converters within last 2 years - Positive Skin Test reactor with chest X-ray findings consistent with non-progressive TB with whom there are neither positive cultures no a history of adequate chemotherapy - HIV-infected person with high risk previous TB exposure especially when T cells below - Positive TB skin test in special clinical situations |
|
|
Epidemiology of Lung Cancer
|
- Tobacco
- Genetics, radon gas, asbestos, metals and industrial carcinogens, thoracic radiation therapy |
|
|
Types of Lung Cancer
|
- Respiratory Epithelium Based
- Adenocarcinoma - Squamous Cells - Small (Oat) Cell - Large Cell |
|
|
Clinical Presentation of Lung Cancer
|
- Asymptomatic
- General - Weight Loss, Asthenia, Anorexia, Change in Cough - Central/Endobronchial - Cough, Hemptysis, Wheeze, Stridor, Dyspnea, Post-obstructive Pneumonia, - Peripheral - Pain (chest wall/ Pleural), Dyspnea (restrictive), Lung Abscess (cavitation) |
|
|
Adjacent Structures affected by Lung Cancer
|
- Tracheal Obstruction - Dyspnea
- Esophageal Compression - Dysphagia - Recurrent Laryngeal N. - Hoarseness - Phrenic N. - Elevation Hemidiaphragm - Sympathetic N. - Horners Syndrome |
|
|
Metastatic Sites of Lung Cancer
|
Brain - Headache, nausea, Neuro
Bone - Pain, Pathologic fracture Bone Marrow - cytopenia, Leukoerythroblastosis Liver - Biliary Obstruction Lymph Nodes Spinal Cord Adrenal Gland |
|
|
Pancoasts Syndrome
|
Suprior Sulcus Tumor/Lung Apex: Alters C8, T1-2
Sholder Pain, Radiation into ulnar distribution: 1st and 2nd rib destruction: Atrophy Arm Muscle |
|
|
Superior Vena Cava Syndrom
|
Vascular Obstruction - Cyanosis of Head, Neck, Arms, Venous Engorgement;
Edema of Face, Arms, Upper Third Thorax |
|
|
Pericardial/Cardiac Extension
|
Tamponade, Arrythmia, Heart Failure
|
|
|
Lymphatic Obstruction
|
Pleural Effusion
|
|
|
Neuroendocrine Properties in Lung Cancer
|
Adrenocorticotropic Hormone - Hypokalemia
Vasopresin - Hyponatremia: water retention: Natriuresis Atrial Natriuretic Factor - Decrease Renin: Natriuresis Gastrin Releasing Peptide - Hyperacidity PTH Related Peptide - Hypercalcemia, Hypophosphatemia |
|
|
Eaton-Lambert Myasthenia Syndrome
|
Progressive Proximal Muscle Weakness in patients with carcinoma
Caused by antibodies directed against the motor-nerve axon terminals |
|
|
Adenocarcinoma
|
- 32% of cases
- Arises from Mucous glands or in the distal bronchial epithelial cells - Usually spreads through the alveoli and may be present as an infiltrate or a single or multiple pulmonary nodule - Most common in Women and Non-smokers |
|
|
Squamous Cell Carcinomas
|
- 29% of cases
- Epithelial cells of the bronchus - Centrally located and usually presents as a mass - May present with hemoptysis and can usually diagnose it with sputum cytology - Spread is loacal so may be able to see it radiographically |
|
|
Small Cell Carcinoma
|
- 15-20% of the cases
- This cancer is of bronchial and obstructs the bronchus. - Hilar and mediastinal abnormalities are common on radiography - Metastasis usual at time of diagnosis - Surgery not curative |
|
|
Large cell Carcinoma
|
- 9% of cases
- Relatively undifferentiated - May Present as central or peripheral masses |
|
|
Bronchial Carcinoid Tumors
|
Tumors of Bronchial Glands or carcinoid Tumors of the bronchials
- Most Patients are under 60 - Bronchoscopy is usually diagnostic - Surgical excision can result in more favorable prognosis |
|
|
Mesothelioma
|
- More common in men
- 60-80% have history of asbestosis exposure - Onset in insidious - highly deadly |
|
|
Diagnosis of Lung Cancer
|
no Adequate screening test for Cancer of the lung
|
|
|
Low Dose Spiral CT in Lung Cancer
|
when combines with PET shows high sensitive in early detection
- tumors under 2 cm that are resected have a survival rate in th 80% range - Problems arise with lesion that are benign - Follow-up PET scan may help distinguish small benign lesions from malignant lesions |
|
|
Cytology of Lung Cancer
|
- Diagnosis needed to be made by histology of tumor
- Can asses by: Sputum, thorancentesis, Bronchoscopy, Fine Needle Aspiration, Mediastinoscopy (node biopsy), thoracotomy |
|
|
Staging of the Cancer
T: |
Tumor Status Descriptor
T - 0 - No Tumor T - 1 - <3 cm in Diameter T - 2 - >3 cm in Diameter |
|
|
Staging of the Cancer N:
|
Lymph Node Involvement Des.
N - 1 Ispsilateral Node Involvement N - 3 Contralateral Node |
|
|
Staging of the cancer M
|
Distant Metastasis Descriptor
M - 1 Distant Metastasis |
|
|
Staging of Cancer:
Assessment of Performance Standard |
0 - Asymptomatic
1 - Symptomatic by ambulatory 2 - Restricted but out of bed more than 50% of the time 3 - Bedridden more than 50% of the time 4 - Totally bedridden |
|
|
Things to look at when stagin
|
Physical Exam: Nodes, bones, skin, hepatomegaly
Labs: CBC, electrolytes, calcium, creatinine, LFTs including alkaline phosphatase Chest Radiography CT scan Pathology TB skin test EKG |
|
|
Treatment of Cancer
|
in Non-squamous cell Lung Carcinoma - resection is the cornerstone of treatment
- also with radiation and then chemotherapy |
|
|
Treatment of Squamous Cell Lung Carcinoma
|
- Tumor Response rates are good with chemotherapy
- Recurrence is common - 2 year survivial is 20% in spite of treatment |
|
|
Palliative Care in Lung Cancer
|
- Focus is on Comfort
- Control of pain - Control of Dyspnea - Control of Delirium |
|
|
Clinical Approach to the Management of Pain
|
- Ask About pain
- Believe the family - Choose pain control appropriate for the patient - Deliver interventions in a timely, coordinated manner - Empower patients and families - Follow up to reassess the pain |
|
|
Solitary Pulmonary Nodule
|
- Most common thoracic radiographic abnormalities
- Aprrox 150,00 cases are detected each ear - 35% of these are malignant - Most are bronchogenic carcinoma but some may be solitary metastases |
|
|
Steps in ruling out maligancy
|
- Compare old films
- Rapid Growth suggests infection, long term stability suggest it is benign - Increase in size suggest malignancy - Ill-defined borders, lobular appearance, high-resolution CT of speculated margins and peripheral halo all suggest malignancy - Sparse calcifications and cavitary lesions suggest malignancy |
|
|
Most common etiology of Pulmonary Metastasis
|
Kidney/Bladder
Breast Colon Cervical Melanoma Testicular Osteogenic & Soft tissue sarcomas |
|
|
Mechanism of Pleural Fluid Accumulation
|
1. Increase hydrostatic Pressure (CHF)
2. Decreased Oncotic Pressure (Nephotic) 3. Decreased Pressure in Pleural Space (like lung collapse) 4. Increased permeability (inflammation) 5. Impaired Lymphatic drainage (malignancy) 6. Communication with peritoneal space and fluid |
|
|
Diagnosis of Pleural Effusion
|
combo of Radiographic procedures, thoracentesis, percutaneous pleural biopsy and thoracoscopy
|
|
|
When can you do a thoracentesis
|
when pleural effusions that do not layer out at least 1 cm are to small to safely perform a thoracentris.
This might be reabsorbed with small amount |
|
|
Thoracentesis
|
Procedure for removing pleural fluid percutaneously
- Initial diagnostic test used to evaluate a pleural effusion of unknown etiology |
|
|
Contraindications for Thoracentesis
|
Coagulopathy
Pleural effusion of insufficient volume Mechanical Ventilation |
|
|
Complications of Thoracentesis
|
bleeding
pneumothora infection puncture of abdominal organs (spleen/liver) reexpansion pulmonary edema pain |
|
|
Exudate lab results
|
- Pleural fluid/serum protein ration > 0.5,
- Pleural fluid / serum LDH ratio > 0.6 - Pleural Fluid LDH>2/3 of upper limits or normal serum LDH |
|
|
Thoracoscopy
|
Pleural biopsy under direct visualization through a thorascope
- high yield for diagnosing both benign and malignant pleural disease, however it required general anesthsia and is usually employed only after other diagnostic procedurs are nondiagnostic |
|
|
What is unilateral pleural effusion prompt?
|
search for another cause of pleural effusion.
CHF usually will have bilateral pleural effusions and have orthopnea, edema, cardiomegaly, pulmonary edema |
|
|
Chemical pleurodesis
|
fusing of the pleural walls togehter
- to treat recurrent pleural effusions most often secondary to malignancies and to prevent spontaneous pneumothorax |
