Reticulocytes and MCV: Mean Red Blood Cell Volume

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Reticulocytes
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Immature red blood cells that still contain ribosomal RNA (look like wavy lines inside the RBC) and nuclear fragments bigger than mature RBC. No bi-concave disc appearance. Normally there are some of these in the marrow and some of these in the peripheral blood
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MCV: Mean Red Blood Cell Volume
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the average size of the RBCs Normal Value - 80-95 fl
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MCV <80 fl
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Microcytosis
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MCV > 95 fl
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Macrocytosis
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Erthyropoietin
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Controls red blood cell production (Erythropoeisis) produced by renal tubule cells in response to O2 saturation in blood
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Normal RBC life span
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120 days
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Causes of Anemia (6)
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Nutritional Deficiencies Congenital Hgb abnormalities Bone Marrow abnormalities Loss of RBC due to bleeding Hemolysis Suppressed Erythropoeisis
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Nutritional Deficiencies that cause Anemia
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1. Iron - stored as ferritin, part of heme. Carries O2. 2. B12 - Essential Vitamin for DNA Synthesis. 3. Folate - Essential Vitamin for DNA Synthesis
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Thalassemia
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defect in alpha or beta globin chains (in HgB). Inherited. Mostly in Mediterranean, Caribbean/African, far east RBCs look like targets (with red middle)
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Alpha Thalassemia
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the HgB acts as a constant spring, and the enlongated protein hemolyzes RBC more frequently.
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Sickle Cell Anemia
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Single-AA mutation in beta chain (Valine for Glutamic Acid), causing the hgB to precipitate and polymerize, causing the rigid elongation. Inherited. Protective against malaria Sub-saharan African, Indian, Arabian Peninsula Unpredictable vaso-occlusal pain crises and strokes
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G6PD (Glucose 6 Phosphate Dehydrogenase) Deficiency
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RBC enzyme that helps keep RBC oxygenated African, Mediterranean, Asian descent most common
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Aplastic Anemia
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empty bone marrow
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What else can the bone marrow be filled with that would interfere with erythropoeisis?
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Leukemia/Lymphoma/other metastatic cancer
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Hemolysis Causes (4)
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Extra-corpuscular Causes Red Cell Membrane Defects Hemoglobin Defects Enzyme Defects
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Autoimmune hemolytic anemia (AIHA)
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IgG-mediated. (spherocytes caused by macrophages taking a bite out of RBCs)
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Red Cell Membrane Defects
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rare. Eg hereditary elliptocytsos or hereditary spherocytosis
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Chronic Causes of Suppressed Erythropoeisis
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1. Renal failure - most common 2. Also - lupus, Crohn's, Rheumatoid Arthritis
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Haptoglobulin
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THIS transfers hemoglobin to liver: if there is increased free hemoglobin from hemolysis, THIS binds to that and the levels of free THIS goes down
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Signs of Anemia
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Pallor Koilonichia Smooth Tongue Tachycardia Bleeding Sx of Bone Marrow Failure Hemolysis Jaundice Splenomegaly
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Koilonichia
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spooning of nails
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Sx of Bone Marrow Failure
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i. Evidence of Severe Infection/Sepsis ii. Bruising iii. Petechiae (usually starting at feet, because lower parts of the body have higher orthostatic pressure, and moving up the body).
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Causes of Jaundice
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When RBC are broken down in circulation, HgB is released. Heme is broken down into bilirubin. Rapid bilirubin increase causes THIS
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Chronic Disease risk factors for Anemia
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i. Discoid Rash (Lupus) ii. Evidence of rheumatoid arthritis, renal failure, severe infection/sepsis iii. Dialysis
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Anemia Labs - CBC
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if more than one cell line is low
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Anemia Labs - #retic high + anemia
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Bone marrow is functioning normally Bleeding Hemolysis Nutritional Deficiency on replacement tx
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Anemia Labs - #retic low + anemia
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Dysfunctional erythropoiesis/bone marrow Bone Marrow pathology chronic disease severe nutritional deficiency (not supplemented)
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Anemia Labs - MCV < 80
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Microcytosis (caused by deficient hemoglobin synthesis): a. Iron Deficiency affects heme b. Thalassemia affects globin chains c. Sideroblastic anemia heme synthesis impaired d. Chronic disease - usually not.
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Anemia Labs - MCV > 95 ("REALLY BIG")
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Megaloblastic Macrocytosis: Caused by DNA Synthesis abnormality a. B12 Deficiency MCV of 128 possible b. Folate Deficiency c. Chemotherapy drugs d. Liver Disease e. Myelodysplastic Syndrome (rare)
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Anemia Labs - MCV > 95 ("Less Big")
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Non-Megaloblastic Macrocytosis: RBCs are big for other reasons (not DNA synthesis). a. Reticulocytosis b. Liver Disease c. Thyroid Disease
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Reticulocytosis (High #retic)
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More immature cells are always bigger. Someone who's just had a bleed will have an elevated THIS, which causes an increase in MCV.
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Anemia Labs - Normocytosis + #retic low
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Primary Bone Marrow Failure - Aplastic Anemia, Leukemia Suppressed Bone Marrow - Renal Failure, Chronic Disease
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Anemia Labs - Peripheral Blood Smear
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i. Microcytes/Macrocytes - look like normal RBCs of unusual size ii. Spherocytes - small RBC with no central pallor iii. Sickle Cells iv. Red Cell Fragments - after-effects of hemolysis v. Acanthocytes - red cells pre-hemolysis, with skinny processes sticking out vi. Elliptocytes - look like normal RBCs, but elongated.
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Direct anti-globulin test = Coomb's test
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To measure IgGs on RBCS (to test for AIHA)
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Hemoglobin electrophoresis
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To identify abnormal HgB
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COPD
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Progressive obstruction and destruction of lung parenchyma leading to decreased elastic recoil, increased compliance, increased airway resistance, irreversible reduction in caliber of small airways, air trapping and lung hyperinflation. Systemic manifestations and increasingly frequent/severe exacerbations
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COPD Risk Factors
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Smoking/exposure to smoke Occupational Exposures Indoor/Outdoor Pollution Low SES, older Age, some genetic factors
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COPD Symptoms
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Dyspnea Chronic Cough Sputum
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COPD Treatment
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Smoking cessation/exercise/self-management SABA prn LAMA (Tiotropium) + SABA prn pulmonary rehab LAMA + LABA + SABA prn If more than 2 exacerbations per year, FEV1 variability > 20%, asthma component, atopy: ADD ICS oxygen opioids (in palliative care)
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COPD Exacerbation Treatment
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At Home: Prednisone (5 days) Increase SABA usage If Admitted: SABA/SAMA (Nebulized) Antibiotics (short course: 5-7 days) CXR - to r/o pneumonia
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COPD Pathophysiology summary
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Inflamed/remodeled airways hypersecretion of sputum causing mucus plugging Small Airway obstruction Dynamic Hyperinflation Alveolar Septae destruction Decreased Airway tethering
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Expiratory airflow limitation
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The pathophysiological hallmark of COPD. Expiratory flow limitations with dynamic collapse of the small airways compromise the ability of patients to expel air during forced and quiet expiration; thus air trapping and lung hyperinflation (overinflation) occurs.
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Air Trapping/ Dynamic hyperinflation
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The principal causes of dyspnea (or breathlessness) in COPD. The physiological mechanism that provides the link between expiratory airflow limitation and patient-centred outcomes.
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Dyspnea in COPD
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a sense of increased effort to breathe, heaviness, air hunger or gasping. Graded with MRC Breathlessness Scale.
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Deconditioning
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Peripheral muscle dysfunction which contributes to exercise intolerance, results from the combined effects of immobility, altered nutritional status, prolonged hypoxia and, possibly, to sustained systemic inflammation.
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COPD Exacerbations
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80% Caused by Infection 20% Caused by environment/medications Sustained (longer than 48 hours) worsening of dyspnea, cough, or sputum production Purulent Sputum indicates possible infection Graded with Gold Staging.
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Barrel-Chestedness
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reconfiguration of the ribcage to contain the over-inflated lungs caused by dynamic hyperinflation Symptom of COPD
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Hypoxemia PaO2 defining values
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<= 55 mmHg OR < 60 mmHg in presence of cor pulmonale
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Bronchiolitis
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small airway disease mural chronic inflammation fibrosis with goblet hyperplasia luminal mucus accumulation obliteration of airway lumen
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Acute Bronchiolitis
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Mostly affects infants, almost always caused by a virus, especially RSV (Respiratory syncytial virus)
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Acute Bronchiolitis - Symptoms
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dyspnea, cough, wheeze, low-grade fever < 3 days, rhinorrhea
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Acute Bronchiolitis - Treatment
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No antibiotics, usually self-limited <14 days If progression to pneumonia, can require hospitalization
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Emphysema
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Parenchymal destruction low expiratory force enlargement of airspaces destruction of alveolar walls damage to elastic fibers in interstitium leading to increased compliance
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Emphysema - Symptoms
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The Pink Puffer progressive dyspnea prolonged expiration barrel chested accessory muscle use often cachexic
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Centriacinar Emphysema
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smoking causes increase recruitment of neutrophils at upper lobe
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Paraseptal Emphysema
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bullae at upper lobe, may lead to pneumothorax
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Panacinar Emphysema
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alpha-1 antitrypsin deficiency leading to destruction of elastin in lower lobe
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Chronic Bronchitis
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Productive cough on most days for ≥ 3 consecutive months per year for at least 2 years hypertrophy and numerous mucus secreting glands in the bronchi increased inflammatory cells in bronchial wall of large airways
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Chronic Bronchitis Symptoms
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The Blue Bloater early onset of cyanosis wheezing crackles late onset of dyspnea
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Chronic Bronchitis Treatment
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Same as COPD
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Bronchiectasis
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Irreversible dilation and damage of a portion of bronchial tree and airway walls loss of normal architecture of the wall accompanying infection mucous cannot be easily removed by damaged or impaired ciliated cells
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Bronchiectasis - Types on CT
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Cylindrical Varicose Saccular NB: CXR is not usually sensitive enough to pick up bronchiectasis
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Bronchiectasis - Causes
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infection impaired drainage (cystic fibrosis, primary ciliary dyskinesia, bronchial tumor) infection precedes bronchiectasis unless there is a tumor or other physical obstruction
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Infections that can cause Bronchiectasis
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Bacterial: TB, atypical bacteria Viral: Pertussis, Measles Immunodeficiency Fungal: eg Aspergillus species
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Causes of Impaired Drainage that can result in Bronchiectasis
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Cystic Fibrosis (tenacious mucus) Primarily Ciliary Dyskinesia Bronchial Tumor (secondary to obstruction)
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Bronchiectasis - Symptoms & Signs
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chronic productive cough recurrent infections copious purulent sputum hemoptysis wheezes/rhonchi clubbing
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Bronchiectasis - treatment
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Antibiotics Bronchopulmonary drainage (clear airway secretions, chest physiotherapy) Bronchodilators
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Asthma
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Inflammatory process that leads to airway injury, which results in airway obstruction and airway hyper-responsiveness (allergy-like process). There is hypertrophy and hyperplasia of smooth muscle cells: bronchoconstriction
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Asthma - Symptoms
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Recurrent episodes of cough (especially at night), wheezing or chest tightness after exposure to airborne allergens, pollutants, exercise or RTI Varies A LOT Better with Bronchodilator Can present with Chronic Cough only.
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Asthma - Risk Factors
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Atopy Environmental/Occupational Exposures - animals, dust Family History of Asthma NB: Smoking isn't a risk factor, but worsens THIS
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Asthma - Physical Exam Signs
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Possible Wheeze on Exhalation Generally Young Onset
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Asthma - Spirometry (PFT)
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Pre-BD: FEV1/FVC ratio Obstructive disease *30 minutes Post-BD: If you see an improvement of 12% AND 200 mL in either FEV1 or FVC*
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Methacholine Challenge
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Measure of Airway Hyperreactivity Asthma: Decreased FEV1 by 20% with less than 4 mg/mL of Methacholine AND history suggestive of asthma Borderline Hyperreactivity: Decreased FEV1 by 20% with 4-16 mg/mL of Methacholine
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Asthma - Sputum Analysis
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Increased #Eosinophil
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Atopy
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allergic pre-disposition. Seasonal allergies, asthma, eczema
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Asthma - Treatment Progression
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Confirm Diagnosis Environmental Controls SABA prn ICS + SABA prn ICS/LABA + SABA prn (or add LTRA) increase ICS/LABA + SABA prn oral CS (Prednisone)
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Why can't you give non-selective (B1/B2) beta blockers (eg propranolol) to asthmatics?
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Because non-selective beta blockers can cause bronchoconstriction
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Canadian Asthma Control Criteria
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Daytime SABA use should be < 4 per week Night time sx should be <1 night/week = none Normal Physical Activity without needing to stop to take SABA DURING activity (before is okay) Mild/infrequent exacerbation No absenteeism due to asthma FEV1/PEF is greater than 85% of personal best PEF diurnal variability less than 15%
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TH2 Pathway
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the prototypical allergic-type inflammatory pathway Responsive to steroids IL4/IL5/IL13 → B lymphocytes → IgE → Eosinophils, Mast Cells, Basophils
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Release of IL25, IL33, and TSLP
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A non-allergic infectious-etiology inflammatory pathway Exposure to viruses/oxidative stress can trigger THIS, which can induce BOTH the TH2 and TH17 pathway
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v. TH17 Pathway
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The Neutrophil Reaction: A non-allergic infectious-etiology inflammatory pathway NOT RESPONSIVE TO STEROIDS The T Lymphocyte differentiates TH17, which stimulates neutrophils
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Which inflammatory pathway is NOT responsive to steroids?
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TH17
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Sleep Apnea
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repeated cessation of breathing for > 10 seconds during sleep
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Sleep Hypopnea
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breathing amplitude goes down and then comes back up with periodicity
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Sleep Hypoventilation
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sustained reduction in breathing associated with hypercapnia and hypoxemia
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Central Apnea
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no respiratory effort
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Central Apnea - Causes
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Hypercapnia "Idiopathic" CNS lesions CHF
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Obstructive Sleep Apnea
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respiratory effort against airway obstruction
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How does Obstructive Sleep Apnea affect sleep?
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Sleep Fragmentation Repeated Hypoxia-reoxygenation
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Mixed Apnea
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Starts as central apnea (no effort) and finishes as obstructive Loss of drive to breath causes the airway to collapse. The increase of effort reflects the obstructive effect
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Sleep Apnea Risk Factors
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Obesity Craniofacial abnormalities Family History Smoking currently Nasal congestion
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Sleep Apnea Symptoms
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loud snoring systemic/pulmonary hypertension arrhythmias morning headache nocturia nocturnal choking excessive daytime sleepiness impaired memory/concentration mood disturbances, eg depression increased motor vehicle/workplace accidents possibly sudden death. Patients will complain of fatigue during the day despite a normal amount of sleep
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Sleep Apnea Treatment
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Weight loss/surgery, CPAP, Mandibular advancement prostheses, recommend position change during sleep, hypoglossal nerve pacemaker, avoid alcohol and sedatives
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Micro-arousal
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transient disruptions of sleep, lasting at least 3 seconds but no more than 15 must be BOTH a burst of EEG activity AND a burst of EMG
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Cheyne-Stokes Respiration
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cyclic Incremental, then decremental breathing pattern with no-effort apneas in between
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How does CHF cause Cheyne-Stokes Respiration?
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there is a delay between the changes in PCO2 in the alveoli and at the chemoreceptors because the blood is travelling slowly. Consequently, as you end a breath, the PCO2 at the chemoreceptor isn't low enough to trigger another breath, so this causes an apnea
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Cheyne-Stokes Respiration with Adaptive Servo-Ventilation
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SaO2 and HR will stay level, but the mask pressure will show the Cheyne-Stokes pattern
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Restrictive Lung Disease - Spirometry (PFT)
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decrease in TLC, RV, FRC, VC, Compliance INCREASE in PEF FEV1/FVC normal or >0.80
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Sarcoidosis - Symptoms
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progressive dyspnea short-rapid breaths fever polyarthritis erythema nodosum can be asymptomatic
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Sarcoidosis - CXR
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non-necrotizing granulomas and bilateral hilar adenopathy +/- interstitial pattern often found as incidentaloma
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Sarcoidosis - Epidemiology
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More common in black women
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Sarcoidosis - Etiology
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idiopathic
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Sarcoidosis - Treatment
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PRN steroids, anti-malaria agents, chemotherapy agents
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Interstitial Pulmonary Fibrosis (UIP)
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idiopathic alveolitis followed by fibrosis from pneumonia or occupational hazard or asbestos or silicon (pneumoconiosis)
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Interstitial Pulmonary Fibrosis (UIP) - Symptoms
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Onset in middle-age dyspnea dry cough clubbing rapid & short breathing May be associated with inflammatory disease processes like rheumatoid arthritis, scleroderma, lupus
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Interstitial Pulmonary Fibrosis (UIP) - Prognosis
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5 years mean survival time from onset of symptoms
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Interstitial Pulmonary Fibrosis (UIP) - Treatment
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improvement in 1/3 of patients with steroids
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Pneumonia - Prevention
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Vaccination for influenza pneumococcal vaccine smoking cessation
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Pneumonia - Symptoms in Elderly
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change mental status confusion loss of appetite
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Pneumonia - Physical Exam Signs
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Tachypnea Hypoxia, cyanosis in severe cases Auscultation: crackles, wheeze, decrease in breath sounds Egophony (saying E sounds like A) Whispered pectoriloquy = transmission of whispers due to consolidation Tactile fremitus = Increased sensation of sound by examiners palms Percussion = dull
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Typical Pneumonia, eg Streptococcus pneumoniae - Symptoms/Signs
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Acute onset Rusty color sputum and Dyspnea High grade fever (≥ 38 °C) Shaking chills Pleuritic chest pain
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Typical Pneumonia, eg Streptococcus pneumoniae - Pathology
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Gram-positive diplococci Inflammatory exudate (edema) fills alveolar space, spreads between alveoli Empyema, Bacteremia possible
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Typical Pneumonia, eg Streptococcus pneumoniae - Imaging
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CXR: lobar consolidation and air bronchograms Edema restricted to alveolar space
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Typical Pneumonia, eg Streptococcus pneumoniae - most common in:
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elderly smokers during the holidays 90% of cases community-acquired Very common, but not very infectious
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Other Bacterial Pneumonia, eg Staph. Aureus - Pathology
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Gram-positive bacterium clusters Airways involved Rapid Spread Necrosis and Cavitation Tissue Destruction Empyema Abscess
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Other Bacterial Pneumonia, eg Staph. Aureus - Imaging
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CXR: no air bronchograms (see fluid line), patchy diffuse lobar distribution, necrotizing cavitation. Frequent pleural effusion. CT: bronchopneumonia, multi-lobar involvement
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Other Bacteria Pneumonia, eg Staph. Aureus - Most Common in:
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nocosomial or post-influenza pneumonia in elderly, children Most common cause of death in influenza epidemics NB: Risk of multidrug-resistance bacteria (MRSA, VRSA)
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Atypical Bacteria Pneumonia, eg Mycoplasma Pneumonia - Most Common in
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Young healthy adults Seasonal (fall and winter)
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Atypical Bacteria Pneumonia, eg Mycoplasma Pneumonia - Symptoms/Signs
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Slower onset "walking pneumonia" = often mild headache sore throat myalgia occasional bullous myringitis (ear drum infection) Sx can be confused with viral illness
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Atypical Bacteria Pneumonia, eg Mycoplasma Pneumonia - Imaging
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CXR: interstitial (reticular) pattern bilateral/diffuse CT: ground glass opacities, nodules
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Influenza Pneumonia - most common in
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Elderly with chronic diseases Elderly living in nursing homes Children
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Influenza Pneumonia - Symptoms/Signs
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Flu-like illness (fever, sore throat, myalgia, lethargy, flushing) Dry cough acute respiratory distress syndrome
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Influenza Pneumonia - Imaging/Labs
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CXR: Multi-focal Diffuse interstitial Reticulonodular Ground glass opacities Similar to "atypical" bacteria pattern Labs: Low/mild elevated WBC Sputum with minimal bacteria/neutrophils
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Influenza Pneumonia - Pathology
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Can cause interstitial pneumonia/diffuse alveolar damage
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Aspiration Pneumonia - Most common in
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Elderly Altered Mental Status Alcoholism Neurological deficits (stroke, seizure, head trauma) Vomiting
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Aspiration Pneumonia - Pathology
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Too much mouth/gastric content aspirated Gram-negatives (oral/enteric), Anaerobic microorganisms Often Polymicrobial Multi-drug resistance and abscess formation in most cases
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Why does Aspiration Pneumonia more commonly affect the right lung?
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Microbes affect the areas where they're most likely to land (depends on body position of patient) Anatomically, the right bronchus is straighter down in an upright person --> right-side predominance.
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Aspiration Pneumonia - Symptoms/Signs
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Foul-smelling/tasting sputum Foul-smelling breath (because anaerobes smell really bad)
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Aspiration Pneumonia - Imaging
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CXR: Predominantly right side Gravity-dependent regions Pleural involvement Cavitation possible
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Pseudomonas Aeruginosa - Most commonly In:
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mostly in immunosuppressed patients
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Pseudomonas Aeruginosa - Symptoms/Signs:
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Green sputum Noxious breath Extremely dangerous - need to isolate Multi-drug resistance and abscess formation in most cases
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Pseudomonas Aeruginosa - Imaging/Labs
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CXR: Variable appearance of lobes Pleural Fluid Analysis via Thoracocentesis: test for complicated/empyema
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Pleural Fluid Analysis via Thoracocentesis - Empyema
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pH < 7.2, loculated, pus, bacteria, protein/LDH high
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Pleural Fluid Analysis via Thoracocentesis - Complicated Exudate
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pH < 7.2, +/- loculated, serosanguinous, +/- bacteria, protein/LDH high
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Pleural Fluid Analysis via Thoracocentesis - Uncomplicated Exudate
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pH >7.2, free flowing, serosanguinous, sterile, protein/LDH high
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Pleural Fluid Analysis via Thoracocentesis - Transudate
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pH >7.2, free flowing, serous, sterile, protein/LDH low
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What does "Severe" Pneumonia look like?
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a. Respiratory failure (eg hypoxemia) b. Sepsis (eg low BP, multi-organ failure) c. Extensive Pneumonia on CXR d. Complications, eg pleural effusion/cavitation e. Abnormal labs (hyponatremia, anemia, very low/high WBC, renal failure) f. Other factors: extrapulmonary infection, renal failure, dehydration, mental status change, inability to eat
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Lung Cancer - Major Risk Factors
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Smoking Chemical/Mineral Exposure Radiation Exposure PMHx: Cancer
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Lung Cancer - Symptoms
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Cough Chest Pain hemoptysis neck nodes hoarseness Swallowing problems
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Superior Vena Cava Obstruction (SVCO) Syndrome
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when the SVC has been invaded by tumor, collateral veins develop on the anterior/posterior chest to compensate. Also, facial swelling
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Pancoast Syndrome
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hand or arm pain from brachial plexus involvement Tumor at the apex of the lung can invade the neck/shoulder area
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Horner's Syndrome
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miosis (constricted pupil), partial ptosis (weak, droopy eyelid), anhydrosis (decreased sweating), w/ or w/o enophthalmos (inset eyeball). Caused by damage to the sympathetic trunk
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Disseminated Disease (Metastases) Symptoms
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weight loss, bony pain from mets, headache from mets, soft tissue masses, skeletal Sx, focal neurological deficits
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Squamous Cell CA - risk factors
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SMOKING ANYTHING that will injure the epithelium of the lung is a risk factor. o Smoking anything o GERD/Trachea-Esophageal Reflux o Alcohol abuse o Airborne Chemical/Particle/Pollutant exposure
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Squamous Cell CA - Pathology
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Grows from the epithelium INTO the LUMEN of the proximal lobar airways, occluding them Necrosis can eat away at blood vessel walls causing hemoptysis or bleeding out Keratin in the lumen Intercellular bridging within the epithelium
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Squamous Cell CA - Imaging
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CXR: obstructive pneumonitis: a lesion from the sternum to the periphery which reflects the mass growing in the proximal airway
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Small Cell CA - Key Features
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Very aggressive cancer (2-3 months of life after diagnosis) Almost exlusively in smokers Paraneoplastic Syndrome
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Small Cell CA - Pathology
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Spreads from Bronchial epithelium INTO the SUBMUCOSA, hence why we don't catch it until it is too late (little to no earlier hemoptysis or occlusion) Metastasizes via the lymph nodes and visceral pleura
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Small Cell CA - Imaging
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CXR: dense mass in the hilum CT identifies a widening of the lymph vessels
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AdenoCA - Risk Factors & Key Features
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GLAND PROLIFERATION DISORDERS AND ASBESTOS most common form of cancer (Including smokers and non-smokers [< 100 cigarettes/life]
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AdenoCA - Pathology
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Mostly located on the periphery of the lung Large amounts of gland formation Identifiable fibrous tissue pearls within the large airway folds
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AdenoCA - Imaging
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CXR: nodule on the periphery of the lung
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Large Cell Carcinoma
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Hyperchromicity with a LOT of cytoplasm Usually peripheral, but variable Accompanied with a lot of necrosis in general
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Bronchioalveolar AdenoCA
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spreads along alveolar walls and can look like pneumonia
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Pulmonary Embolism - Symptoms and Signs
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Sudden dyspnea • Chest pain • Hypoxia (low O2 saturation) • Hypocapnia • Hyperventilation • Hypotension (low BP) • Pleural friction rub • Elevated jugular venous pressure • Edema • Tender, swollen lower limb (indicative of deep venous thrombosis
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Pulmonary Embolism - Usual History
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The story is usually one where a patient has been immobilized for a long period of time without DVT prophylaxis (in the case of hospitalized patients) or on a long flight. Patients taking medications predisposing them to be hypecoagulable are also at risk (for example, those on a birth control pill).
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Pulmonary Embolism - Diagnostic Tests
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CT Pulmonary Angiogram CXR: Hampton's Hump, Westermark Sign Blood gas: respiratory alkalosis due to hyperventilation (to increase alveolar ventilation)
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Hampton's Hump
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wedge-shaped defect at pleural edge representing an infarct
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Pulmonary Embolism - Treatment
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begin as soon as suspected: IV unfractionated heparin or SC low molecular weight heparin (LMWH) bridge to PO Warfarin for 3-6 months + supportive therapy to ensure vital signs are stable - oxygen, fluid, vasopressors Also possible - Thrombin inhibitors Factor Xa inhibitors, eg Rivaroxaban
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Pneumothorax - Signs/Symptoms
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• Chest pain • Dyspnea • Chest expansion • Hyper-resonance upon percussion
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Pneumothorax - Types
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• Spontaneous: accumulation of air in pleural space!trachea deviates towards collapsed lung • Tension: Trauma or lung infection!trachea deviates away from collapsed lung!EMERGENCY to salvage the lung not affected
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Active TB - Risk Factors
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Interval since Infection = Highest risk within 1-2 years after acquiring primary infection. HIV/AIDS - Strongest Known Risk Factor. Contraction will make risk increase, even with a long interval since infection Diabetes, Renal failure (especially if on dialysis) Immunosupression (eg transplantation) Age (0-5, elderly) Smoking, alcohol use Under-weight (including gastrectomy) Silicosis
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Most contagious form of TB
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Laryngeal
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Moderately contagious TB
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Pulmonary a. AFB Smear positive, Cavitation on CXR b. Often in younger, male patients c. Patients who cough more
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Less contagious TB
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Minimal Pulmonary a. Smear negative, non-cavitary disease on CXR, older
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Non-contagious TB
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Extra-pulmonary TB
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Active TB - Symptoms
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productive cough for weeks to months, fever, sweating at night, hemoptysis (late in course)
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Active TB - Physical Exam
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Chest exam usually normal. May have low-grade fever, may look thin/badly nourished, may have lost weight
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Active TB - CXR
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Cavitations Airspace Opacities, Air Bronchograms Look especially closely at apices
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Active TB - Sputum Smear
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Smear Positive (~50% of active TB Cases) More likely to be positive in patients with a lot of symptoms
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Active TB - Cultures
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Culture Positive
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Active TB - Nucleic Acid Amplification
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PCR Positive
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Active TB - PPD/TST
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Positive = >5 mm after 3 days
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Active TB - IGRA
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Positive
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Active TB - Treatment
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Legally compelled multiple drugs needed to prevent drug resistance at least 6 months
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Latent TB - Treatment
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Not everyone needs treatment Individual Decision to treat Single drug therapy adequate Standard treatment is Isoniazid for 9 months, Effective but associated with toxicity, so completion is poor New: Rifampin or Combination of Isoniazid/Rifapentine (3-4 months, 1/week)
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MDR-TB
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Multi-drug resistant TB 1. Resistant to INH, Rifampin 2. Mortality >80% 3. Hospital and Community Outbreaks in NYC in 1989 4. Many patients were HIV+ and/or healthcare workers
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XDR-TB
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Extensive Drug Resistance 1. Resistant to INH, Rifampin + 2 most effective second line drugs 2. Mortality: 59/60 patients with HIV died within 6 months 3. Emerged in Tugela Ferry, South Africa, 2005
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TDR-TB
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Total Drug Resistance 1. Resistance to all anti-TB Drugs 2. Mortality: 100% of patients, all HIV - 3. Emerged in 2011 in Mumbai
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Mycobacterium avium
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M. Avium is most frequently associated with human disease in Canada, and it may be more prevalent than TB. Often seen in people with previous underlying lung disease (CF, other forms of bronchiectasis, including scarring from old TB). Disseminated disease more common in people with advanced, uncontrolled AIDS
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Mycobacterium avium - symptoms
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Indolent Sx: cough, sputum, weight loss over many months Intermittent hemoptysis, moderate exercise-induced SOB possible CXR: nodular lung infiltrates associated with bronchiectasis, cavitary lung disease Disseminated THIS Disease a. Systemic/GI Sx (diarrhea) b. Pulmonary/Lymph Node involvement c. Can culture THIS from blood.
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Mycobacterium avium - treatment
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Not mandated. Depends on species. Much longer than standard TB treatment. Difficult to tolerate Requires 3-4 drugs Not consistently effective
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Dyspnea
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Subjective experience of breathing discomfort Comprised of Qualitatively distinct sensation (ie "choke" vs "wheeze" vs "can't breathe enough in" vs "feels like a snake moving in my lungs")
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Factors that contribute to Dyspnea
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i. Physiological ii. Psychological (anxiety) iii. Social (performance anxiety) iv. Environmental (claustrophobia, light sensitivity)
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Dyspnea - Treatment
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a. Best option = treat the cause b. If the cause is recalcitrant = treat the symptom Oxygen has little effect beyond placebo Diagnosis and ethical considerations guide the treatment Even if the patient is old and/or is sure they're going to die, they may be wrong You have to respect what the patient has expressed/documented in wishes for end-of-life care Palliative care is a continuum that starts early. There is always a balance between palliative care and curative/restorative care. Pleural fluid requires specific intervention
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Cough
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can also be psychological can be neurologically controlled, local respiratory medicine will be ineffective Cough center responds to opiates
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How to convert oral to subcutaneous dosing of morphine:
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Calculate oral dose for equivalent of 24 hours. Divide by 2 --> subcutaneous Divide by 6 --> for injections q4h
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Cystic Fibrosis - Pathogenesis
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Defective CF gene Deficient CFTR protein Decreased chloride secretion/altered ionic transport Increased water absorption/abnormal mucus composition Bronchial obstruction Bacterial infections Inflammation Bronchiectasis and Lung Insufficiency
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How does Cystic Fibrosis affect the respiratory epithelium?
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No chloride, sodium, water secreted --> dehydrated layer Mucus sits directly on cilia Because lack of water --> mucus is thicker and stickier Attaches to airway --> causes infection/inflammation
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Cystic Fibrosis - Clinical Symptoms/Signs
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Recurrent Respiratory Infections Sinus Disease - panopacification of paranasal sinus by 8 months Chronic rhinosinusitis Pancreatic Disease - insufficiency from birth. Steatorrhea, malnutrition, failure to thrive Fat-soluble Vitamin Deficiencies (AEDK) Meconium Ileus (small bowel obstruction at birth) Distal Ileal Obstruction Syndrome (small bowel obstruction) Liver & Biliary Disease in Males - infertility secondary to congenital absence of vas deferens in Females - secondary amenorrhea, abnormally tenacious cervical mucus
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Cystic Fibrosis - Diagnosis
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Collection of Sweat with Pilocarpine Iontophoresis - chloride > 60 Genetic panel for CFTR mutations Gene sequencing
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Cystic Fibrosis - Treatments
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Mostly Symptomatic- Antibiotics Bronchodilators Chest physiotherapy DNAse new therapies targeting specific mutations (Ivacaftor, Lumacaftor)
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