M2 Pulmonary Week 3 - Key Facts Flashcards
TB Microbiology Key Points (4)
1) Aerobic (Like’s Top of Lungs) Mycobacteria
2) Bacillus
3) Non-Spore Forming
4) Cell Wall has Mycolic Acid (Acid Fast Stain)
Outcomes Following Infection (3) + %
1) Primary TB - 5% - Lower Lobe + Serious
2) Latent TB - 80% - Never Symptomatic Again
3) Reactivation TB - 10% - Get it again later
Risk Factors for TB Reactivation (5)
1) HIV
2) Immunocompromised
3) Renal Failure
4) Diabetes - Exam Key
5) Silicosis
Gross Imaging Findings (2) + Histology Findings (2)
Gross Ghon Complex (Lower Lobe) - Calficifcations + Fibrosis - Gray/White Lesion
Histology
1) Caseating Granulomas
2) Epithelial Histocytes - High Calcium
PPD - Test Basics (3)
1) 48-72 Period then reexamine + only measure the bump not the redness
2) Triggers Type III (IgG) Hypersensitivity Reaction
3) Positive PPD = TB at some point (but may be latent)
PPD - 3 Cut Off Points
1) < 5 mm - Immuncompromised (Lose ability to respond to Type III so any response is note worthy) - HIV/Transplant
2) < 10 mm - Risk Factors - Immigrants + IV Drugs + Kids + Healthcare Workers
3) < 15 mm - Everyone else
Interferon Gamma Release Assay - Key Points
1) Draw blood and put it into a vile with TB Antigens - Look to see if patient’s blood makes IFN-Gamma
2) Less interpretation + no follow-up
3) No impact of BCG (TB Vaccine)
Differentiation of Caseating Granuloma (2)
1) Fungi
2) TB - AFB (Acid Fast) = Red = Positive
Signs of Active TB (5)
1) Fever
2) Night Sweats
3) Cough
4) Hemoptysis
5) Weight Loss
6) Gradual
7) No Abx Response
Extra-Pulmonary TB (4)
1) Cervical Lymph Nodes
2) Joints - Potts + Spine
3) Kidney (Sterile Pyuria)
4) TB Meningitis
Miliary TB - Key Points (3)
1) Hematogenous Dissemination of TB
2) Occurs with Primary and Secondary TB
3) Diffuse Nodules on CXR
TB CXR - 3 Types
1) Primary = Lower/Middle Lobe Infilitrates
2) Reactivation = Apical Cavitation
3) Miliary = Diffuse Nodules
HIV TB - 2 Keys
1) Can Have Normal CXR
2) Extra Pulmonary Symptoms More Common
Children TB - 2 Keys
1) Less likely to have cavitation
2) More likely to have intrathoracic adenopathy
CF - Gene Knock-Out + Results
1) F508 = Complete Knockout
2) G551D = Partial = Kalydeco Tx
1) Inflammation + Bronical Obstruction + Bronchiestasis
CF - Diagnosis Criteria (6)
Need 1 In Each Category
1) >1 Phenotypical CF Feature
2) Sibling with CF
3) Positive Newborn Screening Test
1) High Salt Sweat Test
2) IDed CTFR Mutation
3) Abnormal Nasal Potential Different
CF - 4 Major Pulmonary Symptoms
1) Recurrent Pneumonia
2) Atypical Asthma
3) Nasal Polyps
4) Pseudomonas
CF Asthma has clubbing - Normal does not
CF Infection - 3 Key Points
1) Can’t Keep Kids Together
2) Psuedomonas before Age 6 = Bad Prognosis
3) Psudomonas loves the mucous
ARDS Pathophysiology
Diffuse Alveolar Damage –> Due to protein rich fluid leakage + formation of hyaline membranes - Actication of neutrophils causes free radical destruction of Type I and II Pneumocytes
Major ARDS Clinical Features (5)
1) Hypoxdemia
2) Cyanosis
3) Respiratory Distress
4) Dyspnea (Alveoli Collapse
5) White Out CXR
Typical ARDS Causes (8)
1) Sepsis
2) Pulm. Infection (Pneumonia)
3) Shock
4) Trauma
5) Aspiration
6) Pancreatitis
7) DIC
8) Hypersentivity Reactions
Major Stages of ARDS (3)
1) Exudative Phase 1-7 Days
2) Organizing Phase 7-14
3) Resolution Phase
Exudative Phase - Pathophysiology Steps (5)
1) Insult Triggers Inflammation
2) Endothelial + Alveolar Injury
3) Increased Permeability (Protein rich interstitial and alveolar edema)
4) Atelectiasis/DAD
Exudative Phase - Results (5)
DAD
1) Edema
2) Hyaline Membranes
3) Hemorrhage
4) Neurtophil Invasion
Also Type 1 Pneumocyte Destruction
Organizing Phase - Key Points (4)
1) Type II Pneumocyte Proliferation
2) Granulation and fibroblast proliferation
3) Still Reversible
4) Less Hemorrhage on Histology
Resolution Phase - 3 Outcomes
1) Full Resolution
2) Stable Fibrosis
3) Progressive Fibrosis
Collagen deposition = irreversible step
ARDS Rule Outs (3)
1) Localized to 1 Lobe
2) Death within 1 week (underlying cause)
3) Sepsis = Big Cause
Major Pathophysiology Changes in ARDS (4)
1) Impaired Ventilation (loss of alveoli)
2) Surfactant Inactivation
3) Decreased Compliance (Restrictive Lung Disease)
4) V/Q Mismatch - Blood passes through without gas exchange (atelectasis + thick diffusion barrier) - Physiological Shunting = Not responsive to O2
Ventilation Injury Types (4)
1) Barotrauma - Macroscopic
2) Volutrauma - End Inspiratory Volume Over distension
3) Atelectotrauma - Not enough PEEP
4) Biotrauma - Biochemical Injury
Ventilator Injury - Barotrauma + Causes (2)
Macroscopic compression
1) Pneumothorax
2) Subcutaneous Emphysema
Ventilator Injury - Volutrauma + Causes (1)
Large tidal volumes - Causes over extension of the alveoli after inspiration (increases wall stress)
Methods to Avoid Ventilator Induced Injury (3)
1) Optimal PEEP
2) Low Tidal Volume
3) Prone Position
