pulm
Pathological shunt
Caused by impaired gas diffusion b/w alveoli and blood -- b/c thicker diffusion membrane (fibrosis), edema, etc. Results in an increased A-aPO2 gradient b/w alveoli and capillary (A-a) b/c blood passes through the capillary before it gets fully equilibrated with the alveoli. Diffusion of O2 is more affected than CO2 b/c of the lower solubility of O2. This A-aPO2 difference is more prominent when there is higher pulmonary blood flow such as in exercise and with hypoxia. * from boards & beyond
croup—>
Caused by parainfluenza. Steeple sign (narrowing of the subglottis) on X-ray
Vital Capacity—>
Volume of air that can be exhale after a maximum inspiration. VC=IRV+TV+ERV
Inspiratory Capacity (IC)—>
Volume of air that can be inhale from the end of a TV. IC=TV+IRV.
8. Please be able to identify the volumes and capacities from a spirogram. 4 volumes and 4 capacities
(5)
4. Outer membrane
(G- bacteria only)
12) List the different chemical forms of carbon dioxide transport.
(IN RED) CO2 (dissolved) + H20—> H2CO3 (Carbonic acid)—> H+ + HCO3- (bicarbonate) R-NH2 + CO2—> HN-R-NCOO- (Carbamino group) + H+
Normal mastoid
(best assessed laterally): Bony septae are relatively thin, mastoid air cells filled w/air not fluid
CAUSES OF AIRWAYS OBSTRUCTION: Ludwig's angina
(cellulitis floor of the mouth // basically swelling of tissue that will obstruct upper airways). Tonsilitis
Sigmoid Sinus Thrombosis
(feared complication of Mastoiditis): Lecture 25 Week 2: Hemoptysis
Conduction Airways defenses Mechanical barriers
(larynx) and airway angulation Defects Endotracheal Tube Tracheostomy Potential infection problem Aspiration: Direct entry of microorganisms into distal airway
Cells: Agranulocytes:
(w/o granules) Mainly adaptive immunity B cell, T cells Natural killer (NK) cells—> Innate immunity!! immune surveillance, destroy virally infected cells, tumors through Antibody-Dependent Cellular Cytotoxicity (ADCC) or release of perforin—>granzymes—> caspaces cascade—> cell death.
B. Cell envelope (G+ and G-) and possible appendages 1. Inner cell membrane
- none (no organelles)
DNA repair
- not a permanent mutation until sealed in by replication
Review of bacterial genetics Types of DNA involved in bacterial genetic exchange Bacterial Host Genome
- single supercoiled circular, integrates new DNA
3. Explain the various defenses utilized by the innate immune system and the role they play in the immune response (physical barriers, chemical barriers, cells, complement system). Physical barriers
- tight junctions, mucins, cilia, gut peristalsis, normal microbiota
Methods of horizontal gene transfer (HGT) Transformation
- uptake of naked DNA from the environment
Hypoventilation
, alveolar ventilation is at a rate inadequate for the body's demand for O2 consumption or for CO2 elimination. With hypoventilation, the alveolar PO2 ↓ and the PAO2↑(should it not go down? K.w ; c.p said this so idk (HF)), PACO2↑.
Mutagens
- chemical, radiation, viruses
Genetic mutation and repair Spontaneous mutations
- errors in DNA replication, rare
Inversions
- may or may not cause gene expression problems
15) Define and contrast the Bohr and Haldane effects
. Haldane effects—> loss of O2 turns Hb into a weak acid/Strong base, allowing it to attract more H+, buffering the solution. Also, this loss allows Hb to form more carbamino compounds. Bohr effect—> Decrease in affinity of Hb for O2 due to an increase in CO2 and a decrease in pH. The difference here is that for the Haldane effect, deoxygenated Hb attracts more H+ and form more Carbamino compounds whereas in the Bohr effect the high amount of CO2 and low pH increase O2 unloading. Chapter 8 - Control of Ventilation
Normal lung anatomy fields on X-Ray:
1
Be able to convert pressure units between mmHg and cm H2O.
1 ATM=760 mm Hg and 1 atm= 1034 cm H20
Give a synonym for torr.
1 atm=760 torr = 101.3 kPa (kilo Pascals)
Mastoiditis:
Acute: Fluid but still have find bony septae Chronce: Minimal or no fluid and sclerotic thickened bony septae, air cells coalesce to form larger air cell chambers
C. Nutritional requirements
1. Obligate aerobes—require oxygen; cannot ferment 2. Obligate anaerobes—grow only in the absence of oxygen; ATP yield is by fermentation 3. Facultative anaerobes—can respire in the presence of oxygen or an alternate electron acceptor, or ferment in the absence of any electron acceptors 4. Microaerophilic bacteria—many pathogens only like a small amount of O2
B. Staining Gram stain
1. Primary stain - stains all bacteria purple 2. Mordant - iodine -- complexes w/ the crystal purple to form large aggregate within the heated fixed cells 3. Decolorizer: alcohol or alcohol-acetone -- removes from gram negatives but not the gram positives (stay purple). 4. Counterstain - safranin -- stains G- cells pink/red
External intercostals
12 rib articulate with thoracic vertebrae, allowing for rotation Contraction elevates anterior end of each rib, pulling it up toward a horizontal plane Moves sternum upward → contractions prevent ribs from being pulled down during contraction of diaphragm Pump handle motion Tenses and strengthen the intercostal spaces so as to not be drawn in by descent of diaphragm. Paralysis does not prevent ventilation by the diaphragm alone, but prevents deep breathing/coughing. Innervated by T1-T12 spinal nerves
Routine sputum Pulm diagnostic techniques Transtracheal Aspiration
16-18 gauge needle into cricothyroid membrane Recommended : Unable to make sputum,Routine sputum has contaminants, Sputum negative cases (tuberculosis, fungi) Complications: subcutaneous emphysema, significant hemorrhage, paratracheal infx (0.5-0.2% listed high to low)
Anatomy of the Bronchial Tree
23-24 dichotomous subdivisions 11th order and above do NOT contain cartilage Terminal bronchioles are 0.5mm in diameter Respiratory bronchioles and alveolar ducts are membranous and involved in gas exchange
Understand the role of the pulmonary function studies in patient evaluation
4 roles: Establish diagnosis of pulmonary disease and assess severity Document effectiveness of therapy Chart the course of a disease through serial testing Educate patients and facilitate lifestyle alterations
LARGE INTESTINE/COLON:
99.9% anaerobes Bifidobacterium—> GOOD (HIGH #) Lactobacillus—> GOOD (HIGH #) Eubacterium, bactericides, Fusobacterium, clostridium, Strep, enterococcus, Enterobacteriacee.
Minor hemoptysis
: Blood streaks or tinge in the sputum Massive: 150-600mL/4-24 hours 5-15% of all hemoptysis Mortality 71% though drops to <5% if > 24-48 hours NB: Airway volume = 150mL
Accessory structures
: Lymphatic vessels—> reduce swelling and transportation of immune cells.
Pulm infections in AIDS
: gradual onset If normal T-cell count, NOT opportunistic infection, probably normal inf Systemic sx like fever, night sweats, weight loss Pulm sx like dyspnea, cough Most common in <200 T-cell is pneumocystis jiroveci or mycobacterium avium Location is important when considering weirder dx Dx: CXR, ABG indicates severity, HPI important, sputum, transbronchial biopsy
Clinical manifestations rubella
: seperated into transient, permanent, delayed Transient: low birth wieght, thrombocytopenia,HSM, bone lesions, etc.
Extracellular enzymes
= spreading factors Collagenase, proteases, hyaluronidase, DNase
Association (70-100mmHg)—>
A huge change in PO2 has little csq on the Hb saturation. This minimizes the impact of fluctuation PO2 on the O2 in the blood (going hiking...)
11.Contrast primary and secondary immune (antibody) responses in relation to their: i) response (lag) time after exposure to a pathogen, ii) antibody isotype produced, iii) antibody titers, and iv) antibody affinity.
A new, or primary immune (antibody) response, activates many naive mature B cells and stimulates the production primarily of IgM. chronic or ongoing infxn or condition often leads to the production of primarily IgG from memory B cells, however naive mature B cells may still be activated upon second or subsequent antigen exposure. The peak maximum antibody production (titers) is higher and the time required to stimulate an immune response is less in the secondary immune response as compared to the primary immune response. Martin start here
Dissociation (20-50mmHg)—>
A small change in PO2 results in a rapid unloading of O2. This is advantageous for O2 tissue distribution.
17.Discuss the mechanism and benefit of the hapten-carrier effect in vaccine production.
A small, immunogenic component of the bacteria or virus (hapten) is attached to a large protein (carrier), the hapten-carrier complex can activate a hapten-specific antibody response and a carrier-specific Th cell response. I.e; the BCR (B cell receptor, the antibody), binds to the hapten, activating the B cell to endocytose the entire hapten-carrier complex. This complex gets processed and the digested peptides of the carrier portion of the complex are presented into MHC II molecules on the surface of the B cell where they are presented to helper T cells. These T cells are then activated to produce cytokines involved in isotype switching of the B cell. Thus: the hapten-carrier effect can lead to the production of memory B cells which can produce high affinity IgG, IgA, or IgE specific for a non-protein antigen.
4. List the approach in evaluating respiratory failure
ABG in ALL patients suspected to have RF H & PE Use of accessory muscles of respiration Retraction of intercostal space (hoover's sign) Cyanosis Wheezes, rales, rhonchi Asterixis Papilledema coma Sx: dyspnea, tachypnea, confusion, stridor, headache Diagnostics and labs Imaging A-a gradient PFT
Understand how deficiencies in humoral and complement immune systems can lead to certain infections
Ab problems, mostly infections w/ encapsulated bugs Ab or complement deficiency due to hyposplenic or B-cell diseases Antibody def and Complement def ( C3-C9 and alternate pathway, exclude C4 and C6) → recurrent resp and other infx C3/C5 by S. aureus, GNB, S. Pneumoniae C7-9 by Neisseria pneumoniae Alt pathway by S. pneumoniae and salmonella
Other expiration
Abdominus Diaphragm Continued diaphragmatic contraction during early expiration opposes some of the lung recoil and results in slowing of expiration Ensures a smooth transition from inspiration to expiration
2. Identify and anatomically locate the three components of the respiratory control system.
Above
Pleural Effusion:
Absent tactile fremitus Dullness to percussion Diminished vesicular breath sounds
Understand basic host defense mechanisms
Accumulation of secretions can occur w/overproduction, cystic fibrosis, bronchial obstructions Loss/suppression of cough reflex for any reason could lead to aspiration of gastric contents Suppression of mucociliary apparatus either due to impairment of function or destruction of ciliated epithelium (metaplasia) Impaired alv macrophage ability:can lose their bactericidal and/or phagocytic function when exposed to toxins Pulm congestion or edema
ACID-FAST AND IRREGULAR RODS: Mycobacteriaceae—>
Acid fast rods/ M.tuberculosis, M.leprae Filametous, irregular G+ rods—> Nocardia asteroides (partially acid-fast aerobic) // Actinomyces Israeli (not acid-fast, anaerobic or facultative) Lecture 6 week 2: Pulmonary Defenses
Chemical barriers
Acidic pH prevents microbial growth Antimicrobial peptides such as defensins and cathelicidins Lysozyme present in tears, saliva, breast milk, GI, and GU tracts hydrolyzes peptidoglycan in bacterial cell wall Lactoferrin binds free Fe2+ to inhibit bacterial growth Apolactoferrin (without Fe2+) blocks viral entry by binding a viral attachment receptor (lipoprotein) on epithelial cells Surfactants bind to bacteria, viruses, and fungi to increase their phagocytosis Antibodies (Immunoglobulins, Ig) produced by B cells and plasma cells lead to destruction of microbes Plasma proteins are constitutively secreted by hepatocytes Acute phase reactants such as C-reactive protein (CRP) and serum amyloid P (SAP) bind membranes of bacteria and apoptotic cells to activate the classical complement pathway and/or opsonize Mannose-binding lectin (MBL) binds to surface of bacteria, viruses, fungi, and protozoa and activates lectin complement pathway and/or opsonize Complement proteins opsonize, recruit phagocytic cells, and cause lysis of target cells by binding directly or indirectly to surface of cells or pathogens. Involved in all three complement pathways.
Internal Intercostals
Act antagonistically to the external intercostals Contraction compresses the rib cage to decrease antero-posterior diameter of thoracic cage During coughing, contraction prevents bulging of the intercostal spaces
Key mediator of allergic response (immediate hypersensitivity) mast
Activated by allergen cross linking IgE antibodies in multiple Fcer on mast cells Mast cells then release preformed granules that can increase production of lipid mediators and cytokines (tnf-a and IL-1) Both of these cytokines function to increase the production of cell adhesion molecules on endothelial cells thereby promoting the recruitment of leukocytes. Mast cells also produce IL-4 (an eosinophil chemoattractant, plays a role in asthma) and various chemokines which promote leukocyte recruitment and activation. Histamine - local vasodilation of endothelial cells resulting in decreased blood flow and blood pooling (REDNESS, HEAT), and increased capillary permeability (SWELLING) resulting in PAIN. local smooth muscle contraction within the respiratory and digestive tracts (bronchospasm, increased gut peristalsis). Serotonin - causes local vasodilation like histamine Heparin /proteoglycans:temporarily prevent fibrin from forming (inactivate thrombin) Neutral proteases (ex: tryptase) - cleaves fibronectin and type IV collagen (degrade basal lamina of capillary beds) increasing capillary permeability (SWELLING), attract fibroblasts to promote wound healing/scar tissue formation, and activate coagulation cascade to inhibit infection Prostaglandin and leukotriene are lipid mediators released that are stronger than histamine
2. Be able to discuss the pathophysiology of hemoptysis in relation to the structural anatomy and source of bleeding Airway disease
Acute or chronic bronchitis Bronchiectasis Bronchogenic carcinoma Bronchial carcinoid tumor (bronchial adenoma) Other endobronchial tumors (Kaposi sarcoma, metastatic carcinoma)
resp acidosis
Acute uncompensated: pH decreases 0.0075 for each mmHG the PaCO2 is above 40 Compensated: pH decreases by 0.0025 for each mmHg PaCO2 is above 40
2° Lymphoid organs:
Adaptive immune cell activation Lymph node—> B and T cell activation Spleen—> adaptive immune cell response, phagocytosis and opsonization. MALT: comprises G(ut)ALT (tonsils, Peter patches(ileum), vermiform appendix) and B(ronchus)ALT SALT (Skin associated lymphatic tissue)
4. Know management principles in hemoptysis Massive hemoptysis is a medical emergency Airway code
Airway control- prevent asphyxiation Stop the bleeding Buy time to treat underlying disease
18. Apply foundational principles of the lymphoid organs/tissues, immune cells, and the immune response to predict the result if a component is defective or removed.
All discussed in above answers w/ respect to the particular organ/tissue/cell/immune response eg. lack of B cells in agammaglobulinemia, IgA deficiency, splenectomy (loss of B2 cells) etc. Neonatal Respiratory Disorders (2-4 will be answered together as I discuss the various disorders, makes more sense than splitting up)
Mast cells—>
Allergies and inflammation response.
Understand the generation, maintenance and importance of the cohesive forces of the intrapleural space.
Although the lung fills most of the thoracic cavity except for the space occupied by the heart and major blood vessels, no ligaments or other tissues hold or attach the outer lung surface to the inner chest wall. If air is allowed access to the "space" between the outer lung surface and inner chest wall, the lung will recoil away from the inner chest wall and collapse (figure). Collapse of the lung creates a condition known as pneumothorax. Thus, it is important to examine the forces that normally link the outer surface of the lung to the inner chest wall. These forces enable the lung and chest cage to function as a single unit. The outer surface of the lung is covered with a visceral pleura that is juxtaposed to the parietal pleura lining the inner chest wall. The "space" or potential space between the two pleura is termed the intrapleural space. The intrapleural space is occupied by a small amount of fluid. The presence of intrapleural fluid provides cohesive forces that help to join or link the visceral and parietal pleura together. The intrapleural cohesive forces resemble those present when a water droplet is placed between two glass slides. While the two glass slides move over one another very easily, they are difficult to separate perpendicular to their adjoining surfaces. Thus, as the chest wall expands during inspiration, the lung is obligated to follow, so the two structures expand as a single unit. When the respiratory muscles contract to increase thoracic volume, lung volume increases by a similar amount. To preserve the cohesive forces linking outer lung to the inner chest wall, the intrapleural "space" must be kept essentially free of air (gases) or excessive fluid accumulation, as would also be the case in the glass slide analogy. However, unlike the glass slides, the pleura membranes are modestly permeable to gases and water. So, forces must continually operate to maintain the intrapleural space essentially free of gases and fluid to preserve the cohesion between the lung and chest wall. Chapter 3 - Pulmonary Mechanics
Cultures:
Always pathogenic: Aspergillus, Nocardia, Cryptococcus Colonizers: Gram negative bacilli, Staph sp., Candida
5. Identify and describe how sensors detect and send information into the brain stem centers to alter breathing rate.
Answered elsewhere
Superficial landmarks
Anterior Sternal notch Angle of Louis Posterior Spinous process of C7/T1 Scapulae Tip of scapula
IL10
Anti-inflammatory cytokine Down regulates production of TNF-α, IFN-γ and chemokines Allows proliferation of bacteria
Recognize how to diagnose pulmonary infections with microbiology, serology, radiology, and invasive methods Serology
Antibody Tests CMV Legionella: Need acute and convalescent tests= Elisa, RIA for Ag in urine Fungal infections= Not useful
Recognize specific immune mechanisms of lung defenses
Antibody mediated immunity Immunoglobulins Complement Cell-mediated Immunity
Define the apex, base, costal, and mediastinal surfaces of the lungs.
Apex: Upper tip of the lung Base: Area of the lung in contact with the diaphragm Costal: Area of the lung in contact with the rib cage (most of the lung, anteriorly and posteriorly) Mediastinal: Area of the lung in contact with the mediastinum (media part of the lung)
Identify and distinguish the applied and opposing forces of breathing,
Applied forces Muscles of respiration Opposing forces Elastance of lung and chest wall Frictional resistance encountered with tissue or air movement Inertia of lung-chest wall and air in air passages
Describe dynamic compression of the airways during a forced expiration.
At onset of maximal airflow, contraction of expiratory muscles at a given lung volume raises pleural pressure above atmospheric level (+20 cm H2O). Alveolar pressure (sum of pleural pressure and lung recoil pressure) is yet higher (+30 cm H2O). Airway pressure falls progressively from alveolus to airway opening in overcoming resistance. At equal pressure point of airway, pressure within airway equals pressure surrounding it (pleural pressure). Beyond this point, as intraluminal pressure drops further, below pleural pressure, airway will be compressed. With further increases in expiratory effort, at same lung volume, pleural pressure is greater and alveolar pressure is correspondingly higher. (only time when pleural pressure is +) Fall in airway pressure and location of equal pressure point are unchanged, but beyond equal pressure point, intrathoracic airways will be compressed to a greater degree by higher pleural pressure. Once maximal airflow is achieved, further increases in pleural pressure produce proportional increases in resistance of segment downstream from equal pressure point, so rate of airflow does not change.
Give the normal range and list reasons for differences between alveolar and arterial partial pressure of O2 (PAO2 - PaO2).
At sea level PO2 = 159 torr → when inspired it decreases to 149 torr in the trachea b/c water vapor Alveolar PO2 is about 104 torr b/c inspired air is diluted and mixed with alveolar air. -- this is equilibrated with the blood flowing through the lung capillaries. Arterial PaO2 is between 96-100 torr The difference between alveolar and arterial PO2 is called A-a difference. Normally about <14 mmHg or (age/4)+4
10. Describe the general development of the lung bud and its relationship to the gut tube.
At the end of the first month of gestation, a single respiratory diverticulum develops out of the foregut. the respiratory system and the foregut are related embryologically so the lung bud is in direct communication with the foregut. As growth continues, the tracheoesophageal ridges begin to separate the foregut from the lung bud and ultimately form a septum that completely separates the esophagus from the trachea and the lung buds. analogy of the lung bud developing into a balloon: the part of the balloon that's in contact with the fist, the lung bud, is the visceral layer. the other lining of the balloon is the parietal layer. The fist develops into the balloon and the fingers are extensions of the lungs Everything that's in contact with the lung is the visceral layer and everything that's against the body wall is the parietal layer. tracheoesophageal malformations can also happen pictured below the thoracic cavity, gives rise to the pleural cavities and the abdominal cavity which are continuous in utero, but eventually separate. As that lung bud continues to expand, it separates into primary and secondary divisions and continues to divide as it grows into the pleural cavity.
Describe the forces or pressures necessary for the bulk flow of air between the atmosphere and the alveoli of the lung.
Atmospheric Pressure - pressure of gasses in atmosphere Alveolar pressure - Pressure of gas in the alveoli Pleural pressure - Keeps the lungs from collapsing Transmural - The pressure that keeps the lungs distended
Bacteriophage
Bacterial virus Genetic element are able to survive outside host cell b/c protein coat protects the genetic material Infect cells and either: replicate = lysis, or integrate = lysogenic state
Be able to apply history and exam taking skills to specific cases COPD presentation:
Barrel Chest Leaning forward (tripod position) Pursed lips Peripheral cyanosis Supra and infra clavicular retractions Diminished vesicular breath sounds Rhonchi Sonorous on inspiration Sibilant on expiration
Explain why Patm (and PB) decrease with altitude.
Bc the earth's surface is at the bottom of atmospheric sea level that extends upward about 100 miles above the surface. The total pressure decreases with increases in altitude because the height of the air column from the surface of the earth to the end of the earth's gravitational field is reduced. With an increase in altitude, there are fewer gas molecules per unit area
Explain inpatient empirical therapy. ICU patients:
Beta-lactam + Macrolide (IV for both) Beta-lactam + Moxifloxacin or Levofloxacin (IV for both) If pt is allergic to beta-lactam → Aztreonam + Moxi/Levo (IV) IV Beta-lactam include Ampicillin/Sulbactam Ceftriaxone Ertapenem
Explain inpatient empirical therapy. Non-ICU patients:
Beta-lactam + Macrolide (IV or IM for both) Beta-lactam (IV or IM) + doxycycline (IV or PO) Moxifloxacin (monotherapy - IV or IM) pt<65 w/o risk for drug-resistant organism -- give macrolide (monotherapy IV or PO)
Anatomic shunt
Bronchial veins (low O2) anastomosis w/ pulmonary veins (high O2) -- known as bronchopulmonary circulation. Thesbian veins of the left heart that drain to the left ventricle. Both of these add poor O2 blood to the systemic circulation and lower PaO2 compared to PAO2 which accounts for 6-9 Torr A-a difference.
Transient tachypnea (TTN) RF:
C-section, mom DM or obesity CXR: prominent vascular markings(star burst pattern), pulm edema, big lung volume, fluid in fissure
Be able to effectively obtain a history and physical exam on a patient with a respiratory complaint
CC HPI: PPQRSTA Past Personal Hx Medical Surgical Social Medications Allergies Family Hx ROS Cardio GI NMS
Compare the different solubilities of O2, CO2 and N2 in whole blood.
CO2 is 24x more soluble than O2 in body fluids CO2 (most soluble) > O2 > N2 (least soluble) The partial pressure of a gas dissolved in a liquid is directly related to its concentration in the liquid, as stated by Henry's Law. The volumes of O2, CO2, and N2 that can be physically dissolved in water or blood plasma at 37°C, when exposed to 1 atmosphere (760 Torr) of the gas, are presented in the table.
Necrotizing, cavitary or abscess-forming pneumonias
CP: combination of cough, fever, chest pain, and often a large volume of purulent or bloody sputum. Clubbing (see) of the fingers and toe after a few weeks. Multiple small (<2cm) abscesses can develop and we call those necrotizing pneumonias, otherwise larger lesions are called abscesses. PP/causes: preceding primary lung infx, aspiration, neoplasm (cause 2nd infx due to obstruction), septic emboli, traumatic/infective implantation, spreading infx from adj infx of esophagus etc As abscess evolve→ overtake more area of tissue → cavitation Organisms are often either only anaerobes or mixed anaerobes/aerobes Aerobes: K. pneumonia, S. aureus, S. pyogenes Anaerobes: oral flora including Fusobacterium, Bacteriodes, Prevotella, Peptococcus/Peptostreprococcus (gram-positive anaerobic cocci or coccobacilli) species
Understand how deficiencies in phagocytic cells can lead to certain infections
Can chemotax to location but can't properly eat the bugs Chronic Granulomatous Disease, Chediak-Higashi Syndrome, Job Syndrome → recurrent pyogenic infxs of skin and other RES (pulm, bone) sites Catalase pos org (S. aureus, salmonella), GNB, fungus streptococci
D. Diagnostic tests
Can use o2 requirement Catalase → enzyme that breaks down H2O2 Oxidase → cytochrome c oxidase Coagulase, urease, hemolysins, etc
Recognize how cell-mediated immunity protects the lung and against which pathogens
Cell mediated immunity: Depends on T lymphocytes Recruits chronic inflammatory cells Effects cytolysis of virally infected cells Activates macrophages for enhanced intracellular killing Induces granuloma formation Two major mechanisms of T cell functional activity Lymphokine-mediated reactions Cell-mediated cytotoxicity Cytolytic T effector cells (Neoplastic cells, viral infected cells) Natural killer lymphocytes Antibody-dependent cellular cytotoxicity (Macrophages binding to antibody-coated cells)
Stimulation of Central Chemoreceptors
Chemosensitive areas are located along the ventrolateral surface of the medulla near the cerebral spinal fluid of the 4th ventricle of the brain. stimulated by an increase in the PCO2 or H+ concentration, but not O2. more sensitive to changes in the H+ or PCO2 of CSF than of cerebral blood. The blood brain barrier limits access of certain blood constituents, such as HCO3- and H+ to the CSF. not sensitive to changes in the PO2 of cerebral blood or CSF.
Nasopharynx defenses
Ciliated and squamous epithelium Filtering system removes particles 10mm or larger Mucous layer with IgA, IgG to prevent epithelial attachment of bacteria Defects: Poor Nutrition Potential infection problems Colonization with pathogenic GNB Normal colonization is 2-6% 4 days in ICU (40%) Colonization to infection (23%)
Plasmids
Circular double stranded, not as stable as host Rarely codes for housekeeping genes or enzymes Can be conjugative - some encode conjugative transfer genes, some mobilize transfer of other plasmids Properties: fertility, production of toxins, pili, other adhesins, siderophores, resistance to toxic chemicals and Ab resistance!
Parovirus B-19
Clinical: transmission: greatest risk during 1st ½ of preg Maternal ifnx can lead to: misscarrages, hydrop fetalis, IUGR, pleural/pericardial effusions Dx: Serology, PCR, Viral detection in amniotic fluid/placenta tissue TX: supportive, intrauterine blood transfusions
Alveolar pressure of oxygen
Clinically it is often important to calculate the mean PAO2 expected in a patient breathing room air or during ventilation with a gas mixture enriched with O2. The "alveolar gas equation," along with a variety of abbreviated forms of this equation, are used to estimate the PAO2. This equation enables the computation of the expected PAO2 when either the inspired fraction of O2 is changed or the PB is altered.
Pseudohemoptysis
Clues Upper Gastrointestinal Tract Hx: Coffee ground emesis, black tarry stools, nausea and vomiting/retching PE exam: Epigastric tenderness, signs of chronic liver disease: spider nevus, palmar erythema Upper Respiratory Tract HX: Bleeding gums, epistaxis, no cough or sputum, sore throat PE exam: Gingivitis, telangiectasia, pharyngitis, ulceration Peds: Approach to Febrile Infant and Child:
Staph—>
Clustered cocci, Catalase + (Cat+), Coagulase +, B-hemolytic (white halo on red background) and yellow on mannitol agar.
EARS—>
Coagulase-neg Staph (CNS)*, (S.pneumo, P.aeruginosa and enterics— FEW of skin microb)
EYES:—>
Coagulase-neg Staph*, (a-Hemolytic strep, Neisseria and Haemophilus— FEW of nasopharynx microbiota)
Bronchovesicular:
Combination of bronchial and vesicular Expiratory phase is high pitched and as long as or longer than inspiratory phase No distinct pause between inspiration and expiration
Vibrionaceae—>
Curved rods, Glc fermenters, oxidase+ // V.cholerae, V.parahaemolyticus
4. Discuss the three complement systems (alternative, classical, and lectin), including their similarities and differences, and describe how each functions to protect the host from pathogens.
Complement protein binds to cell or pathogen service. Three pathways initiated by different events but all require complement protein 3 After C3 is recruited it is cleaved into C3a and C3b by C3 convertase C3a is an anaphylatoxin that causes inflammation (influx of primarily neutrophils C3b binds the target cell or pathogen, opsonizes it and promotes phagocytosis by neutrophils and macrophages If C3a and b don't C5 convertase and MAC can help C5 is cleaved also into C5a (inflammation) and C5 b which initiates late steps of complaint by recruiting C6-9 that form the MAC which osmotically lysis the cell and can cause damage to the host
Know how to evaluate the flow volume loop pattern in obstructive, restrictive and upper airway obstruction Flow-Volume Loop Analysis:
Completed w/spirometer Analysis may lead to detection of large airway lesions: bilateral vocal cord, paralysis, tracheal tumors and tracheal stricture (not routinely suspected from a routine spirogram) Peak expiratory (PEF) and inspiratory (PIF) flow determined Labeled flow-volume graph:
List and describe the nature of the elastic forces in the lung and chest wall,
Compliance - The ability for the lung to distend and expand Elastic Recoil - The lung naturally wants to shrink back inwards Surface Tension - Forces that allow the lung to follow the chest wall in expansion Chest wall - The chest wall wants to naturally expand
Define compliance and distinguish it from elastance,
Compliance is a measure of the ease of deformation/inflation/distenstensibility Change in V/Change in P Elastance is essentially the opposition to inflation/inspiration Low Compliance = High elastance
7) List reasons why the red blood cell is important in the transport of O2 and CO2.
Contains Hemoglobin that binds O2 and CO2 for a better transport b/c both of them are not highly dissolved in the blood. Increases O2 carrying capacity Contains carbonic anhydrase for conversion of CO2—>H2CO3—> HCO3- Buffers the blood by producing HCO3- and by binding to H+
The muscles are divided into two functional groups: Muscles of Inspiration
Contraction → enlarges chest cavity → expansion/stretching of lung → potential energy is stored in stretched elastic structures of the lung → elastic recoil → expiration
Antigen Tests
Cryptococcus= Latex agglutination Fungal infections (candida, aspergillus) Parasitic infections=Pneumocystis
Understand how deficiencies in various local defenses can cause certain types of lung infection
Cystic fibrosis leads to chronic pulm infections S. auerus, Mucoid Pseudomonas Aeruginosa Immotile cilia (damage from smoking) leads to freq mild resp infx Gram Positive Cocci (GPC), Gram Neg Bacilli (GNB)
Syphilis
DX during pregnancy: RPR or VDRL during preg Seropositive preg considered infected unless adequate therapy and dec titer documented Tx by penicillin if not allergic Earlly onset disease (before 2 years) Epi/PG: Result of transplacental transmission of spirochetes from an infected mother Majority is untreated maternal primary or 2ndary, rest early latent, small number late latent Clinical Placenta: may be large, pale with focal villitis, necrotizing funisitis within matrix of umbilical cord Fetal: Still birth/highly symptomatic: premature, HSM, skeletal/skin abn, pnuemonia, Less affected: HSM, elev alkaline phosphatase, abnl LFTS after tx intiatied Lecture 29: Pediatric Chest Radiology No LOs lecture was just x-rays with some notes 3 components of a good quality chest film Penetration - want to see the spine through the lungs. Rotation Inflation - 8-9 ribs should be visible during inhalation.
5. State the PO2 and PCO2 of dry air, moist tracheal air, alveolar gas, mixed venous blood and arterial blood.
Dalton's Law—> Barometric pressure (Pb) = PN2 + PO2 + Pother gases So Pgas= %gas x Pb O2—> 21% / N2—> 78% / Ar—> 1% Moisten environment we have to account for water vapour pressure which is 47mmHg PO2= .21 x (760-47)= 147 In alveoli we have to account for the PaCO2 and R (V/Q mismatch). PaO2= .21 x (760-47) - 0.8= 100mmHg
Fever:
Def: Fever in the pediatric population is generally defined as rectal temp of 38 C or 100.4 F. Pathogenesis: Fever is caused by the release of endogenous pyrogens into the circulation following an infection or immunologically -mediated event. These pyrogens reach the anterior hypothalamus via the bloodstream and liberate arachidonic acid. Arachodonic acid metabolizes to PGE2 which increases the hypothalamic thermostat. Antipyretics work by altering synthesis of PGE2.
Bronchoconstriction
Defects Hyperactive Airways Intrinsic Asthma Potential infection problem Poor removal of secretions Excessive thick secretions Secondary infection
How to assess the ABNORMAL HILUM
Density: should by symmetric bilaterally Size Contour
CT of Chronic sinus disease
Determine candidate for functional endoscopic sinus surgery Determine extent and location of disease Anatomic variations that predispose to sinusitis Lecture 23 Week 2: Normal CT & X-ray of Mastoid + Pathology
Pathogenicity Islands
Different from the rest of the host genome Carry virulence genes, so found in pathogenic strains Different G+C content than host, flanked by direct repeats, IS or tRNA genes (all indicate HGT) Large (>30kb) Can be unstable Lecture 4 week 2: Normal human microbiota and overview of bact classes
Muscles of Expiration
Expiration is usually passive during normal quiet breathing(eupneic) - elastic recoil of lung chest wall of lung and chest wall.
Conjugation - plasmid mediated
Donor/Male contain F (fertility factor) as a plasmid (Fplasmid) or integrated into the host chromosome (Hfr). F factor encodes for the sex pilus. Recipient/female is F-
Taxoplasmosis
EPI/PG: Parasite, cat= host → humans acquire through food/water/soil with infected eggs Congentital transmission usually as a result of maternal primary infx Clinical:
Congential Varicella
EPI/PG: Risk greatest if maternal varicella in first/early second trimester. Exposure in second half of pregnancy may lead to subclinical varicella and zoster in early life. Infection can lead to fetal/neonatal death if mom acquires infection 5 days prior to 2 days post delivery. Clinical: Fetal death or Varicella embryopathy= limb hypoplasia, cutaneous scarring, eye abn, CNS abn DX: PCR= sensitive/specific/rapid (best) DFA= specific/rapid/less sensitive (best) Viral culture, Tzanck, Serology TX:
RESPIRATORY TRACT: URT:
External nare—> CNS, Strep, P.aeruginosa Nasopharynx—> a-hem strep, enterococcus, commensal Neisseria and Haemophilus, staph and micrococci, anaerobes (peptostreptococcus, veillonella, actinomyces), corynebacterium Fusobacterium) Lower—> Protected by mucociliary blankets (only transient inhaled org encounter there if any.
HIV
EPI/PG: Transmissions: in utero via transplacental infx, intrapartum through exposure to maternal blood, breastfeeding Risk for inc transmission: mother viral load, maternal sxs of AIDS/acute HIV, low CD4; Also worry about obsterics risks Dx: neonates performed by serial evaluation of HIV DNA PCR in blood (birth, 2-4 weeks, 2 months, 4 months, confirmed neg at 12-18 months). Tx: Treatment of maternal HIV with AZT during pregnancy and labor/delivery has reduced transmission rates. Treatment of neonate exposed to HIV consists of AZT during first 4-6 weeks of life. Further antiviral prophylaxis/treatment utilized if mother with higher risk of transmission to neonate. If infection confirmed, further HAART treatment and evaluation.
List the factors that account for the elastic properties of the lung,
Elastic and Collagen Fibers form a knitted fabric quality ½ of elastic recoil pressure Surface tension ½ of elastic recoil pressure
Review Bacterial Physiology Bacterial needs for growth
Energy source - light, oxidation of inorganic and organic compounds Carbon and Nitrogen sources Inorganic ions - iron is essential for almost all bacteria! Mechanisms to solubilize iron from host include siderophores, iron-regulatable outer membrane proteins Essential metabolites - amino acids, vitamins Water (unless spore forming)
IL-12
Enhances CMI to intracellular pathogens Produced by AM, pulmonary epithelial cells, PMN Increased levels resulted in bacterial killing and improved survival
Main differential abnormal hilum
Enlarged vessels tend to taper into lung Tumor may be round and smooth or irregular Lymphadenopathy "bunch of grapes" appearance
Recognize the anatomic lung host defenses of both the upper and lower respiratory tract Upper Resp. Tract
Epiglottis Frequent branching of pulmonary tree: aerodynamic filtration of inspired air Mucociliary clearance of particulates Cough response
CT of Acute sinus disease
Evaluate complications of acute sinusitis To plan surgical drainage When to diagnosis uncertain
Extracellular bacterial proteins: often critical virulence factors
Exotoxins typically secreted using one of the secretion methods listed below (part c) 2 characterizations: activity and structure Activity: where do they act? Ex. neurotoxin acts on the nervous system Structure: 1) AB subunits, A = enzymatically active, B = binds target cell 2) Cytolysins - phospholipases, pore-forming toxins 3) superantigen toxins - act as a polyclonal stimulator of T cells + stimulate B cell differentiation
Abdominal Muscles
External/Internal oblique Rectus and transversus abdominis They increase intra-abdominal pressure to force the diaphragm upward T1-T12 innervation Principal muscles for coughing and forced lung expiratory volume measurements like Vital Capacity
7. Endospores (G+ only)
Extremely heat/drying resistant Metabolically inactive yet viable Lecture 3 (session 2): Micro- Bacterial Physiology and Genetics
Fates and consequences of newly acquired DNA by bacteria
Fates: Degradation by nucleases by restriction modification systems Stabilization by circulation - DNA may become a plasmid Integration into host chromosome - genetic recombination Homologous - recA dependent, significant homology between donor and recipient Site specific - recA independent, occur at unique DNA sequences, involved in the integration of IS elements or transposons Consequences: Phase/antigenic variation Acquisition of antibiotic resistance Acquisition of new characteristics
Fever Categories:
Fever of short duration with localizing signs and symptoms: a dx can be made by H&P. Fever without localizing signs and symptoms: in kids < 3y where H&P fails to dx but labs can suggest dx. Fever of unknown origin: lasts > 14 days and has no etiology despite H&P and labs
Treatment: fever
Fever with temperatures < 39°C in healthy children generally does not require treatment. Antipyretics provide symptomatic relief. Antipyretic tx is beneficial in high-risk patients who have chronic cardiopulmonary diseases, metabolic disorders, or neurologic diseases and in those who are at risk for febrile seizures. Hyperpyrexia (>41°C) : greater risk of hypothalamic disorders or CNS hemorrhage and should be treated with antipyretics. Neonates: Less than 1 month of age All febrile neonates should be hospitalized: - blood, - urine, - cerebrospinal fluid (CSF) should be cultured - Empiric intravenous antibiotics. - Stool culture and chest radiograph may also be part of the evaluation.
DX hilum
For further dx of hilar abnormality after CHXray do CT to determine if abnormal appearance caused by vessel or mass Lecture 22 (session 2): Normal sinus anatomy, sinus x-ray views, and sinus pathology Normal sinus anatomy
6. Predict the effects of alterations in alveolar ventilation and pulmonary blood flow on alveolar PO2 and PCO2.
Functional residual capacity Act as a buffer against extreme changes in alveolar PO2 w/ each breath.
5. Capsule
G- and G+ Usually polysaccharide but can be protein too
Protein secretion systems - review of types and functions
General Secretion Pathway (GSP): Both Grm +/- Proteins targeted to the cell membrane Secreted proteins have N terminal signal sequence cleaved by Lep (post-translational) Signal Recognition Particle (SRP): Both Grm +/- Proteins targeted to the cell membrane - while protein is translated N-terminal signal sequence not cleaved by Lep Grm - specific: Overall 5 place where Grm - can specifically target proteins: 1) Cytoplasm 2) Cytoplasmic Membrane 3) Periplasm 4) Outer membrane 5) Extracellular matrix
Hospital- or health care-associated pneumonias
Generally defined as anything acquired from health care setting Gram-positive cocci (S. aureus and S.pneumoniae) Gram-negative rods (K. pneumoniae and other Enterobacteriaceae, P. aeruginosa) These are most problematic due to their bacterial resistance to antibiotics, such as MRSA, the growing problem of gram-negative resistance, etc. Lecture 16 (session 2): Respiratory and Sinus Radiology
3. Know what factors can affect the composition of the microbiota.
Geography Diet Age Hormonal state Physiological differences Hygiene practices
FACULTATIVE ANAEROBIC G- RODS: Enterobacteriaceae (enterics)—>
Glc fermenters, oxidase- (can respire but do not make cyt c oxidase) // E.coli, enterobacter, shigella, salmonella, klebsiella, proteus, Serratia, yersenia.
Identify etiology. Lower Respiratory Tract Infections: Bacteria pneumonia
Gram + Strep. Pneumoniae - most common Staph aureus - in IVDU and people with debilitating disorders Enterococcus Nocardia Gram - Pseudomonas aeruginosa Klebsiella H. influenzae E. coli Moraxella catarrhalis - an aerobic diplococcus known as the common colonizer of the respiratory tract. Acinetobacter baumannii - associated with VAP Atypical bacteria "walking pneumonia" Mycoplasma Chlamydia Legionella - high mortality if tx is delayed.
Staining tech
Gram stain Acid fast: (Ziehl Neelson, Kinyoun) Mycobacteria India ink: cryptococci Methenamine silver or Toluidine blue 0: cyst walls of pneumocystis Direct fluorescent antibody staining: Legionella KOH - Fungi Papanicolou stains: cancer cells
Kaposi's sarcoma:
HHV8, pleural effusion and bilateral infiltrate, NEGATIVE gallium Tx w/ chemotherapy, prognosis isn't great Lecture 9 (session 2): Hospital Acquired Pneumonia (HAP)
HAP = hospital acquired pneumonia
Half of pts w/ HAP can develop serious complications such as respiratory failure, pleural effusion, septic shock, empyema.
10) Distinguish between hemoglobin saturation, oxygen-carrying capacity, and oxygen content of blood.
Hb saturation—> % of Hb bound to a gas (from the available Hb) O2-carrying capacity—> Amount of Oxygen that can be bound by one gram of Hb O2 content—> Total amount of oxygen present in the blood. E.g—> a decrease in Hb will lead to a decrease in content even if the saturation is 100%
GI TRACT: MOUTH:
Heavily colonized Gums—> Anaerobes (Bacteroides, Fusobacterium, clostridium, peptostreptococcus) S.Aureus, S.epi Neisseria sp Mycoplasma Diphtheroids, lactobacilli a-hem strep, Strep. mutans
Pulmonary (repeat for clarity); symptoms include:
Hemoptysis Dyspnea Orthopnea Cough Fever Night sweats Chills Rigors Chest pain Wheezing Weight loss Sputum production
6) Explain the relationship between the partial pressure of oxygen in blood and the concentration or content of O2 in plasma and whole blood.
Henry's Law—> content of a dissolved gas in a liquid phase is equal to (partial) pressure of the gas in the air phase times the solubility of the gas in the liquid phase. Cgas= Pgas x Solubility. Now in the plasma, the O2 is dissolved: O2 d= 100mmHg x .003mL/dL = .3ml/dl/mmHg O2 is also bound to Hb: O2b= 1.34mL/g x gHb x %saturation Whole blood: O2t= O2d + O2b
Identify the principal site of airway resistance in the entire airway and the tracheobronchial tree,
Highest resistance in mid-size bronchi Cross-sectional area and linear velocity of flow The deeper (smaller branches) in the tree = the higher CXA but lower flow -- more laminar = less resistance Higher (larger branches) in the tree = less CXA but higher flow -- more turbulent flow = more resistance Lung volume and resistance Decreases in resistance when the alveoli are expanded (or high lung volume)
Know how to evaluate a patient with hemoptysis
History Physical exam: Lungs, nose, mouth, pharynx Chest x-ray (CXR) Localizinge.g. a significant finding in less than 40% of patients Malignancy is found in almost 40% of patients with a localizing finding Non-localizing 60% + normal or abnormal but nonspecific Cancer is diagnosed in only 6 to 10% of patients with normal-appearing or non-localizing CXR Basic lab: CBC with differential, PT/INR, type and cross
TLDR aka summary: fever
History and Physical are key to evaluation and management of febrile infants and children. Labs and imaging decided on a case-by-case basis. Most fevers in children are secondary to viral illnesses. Neonates (<1 month) who are febrile need a full sepsis work-up and antibiotics. Febrile 1-3 month olds are stratified by risk based on physical and labs. Certain comorbid conditions place children at higher risk of bacterial infections. Peds: Congential infxs: cases at back lec in CP
4) Specify the relationships of the fissures of the right and left lungs to the thoracic body wall.
Horizontal fissures—> 4th ICS Oblique fissure—> 3rd ICS - 6th ICS (posterior to anterior) Both combine at the 4th ICS mid-axillary (pic)
4. Define nosocomial infection.
Hospital acquired infections
IgE
Host resistance to parasitic, viral infection
Describe the forces governing the movement of gases and fluids between the parietal and visceral pleura,
I think this is what they are asking for → Mainly through the pressure gradients that exist for gases to potentially diffuse.
Define the importance of inertia as a force in opposing lung inflation or deflation,
I'm not sure what its asking - but i think it's answered in the above questions.
Selective IgA deficiency:
Individuals with this immunodeficiency have a defect primarily in the antibody isotype IgA. Individuals with this condition have an increased risk of developing infections in the respiratory and gastrointestinal tracts. The exact cause of this defect appears to vary but mutations in the alpha constant regions of the heavy chain genes of the antibody are thought to be involved. Treatment includes IVIG and antibiotics for treatment of infection.
1. Know the various causes of hemoptysis
Infection Neoplastic Vascular Autoimmune Drug-related and other
Pseudomonas infection emporac - non-ICU or ICU
IV beta-lactam + IV quinolone IV beta-lactam + IV aminoglycoside + macrolide OR quinolone If pt is allergic to beta-lactam → Aztreonam + aminoglycosides (IV) + quinolone
Pulmonary CTA (angiography)
IV contrast Used to detect pulmonary emboli, aortic dissection, aneurysm
Pulmonary angiography
IV contrast injected into the main pulmonary artery and x-rays obtained as contrasts goes thru the PA and its branches. Invasive w/ catheter in main pulmonary artery Large contrast doses can damage kidneys Gold standard for PE Lecture 17 week 2: The Normal Chest
Important aspects of reading a chest x-ray:
Identification of the patient, date of imaging Determine the view (PA, AP, supine) Assess the film quality (proper positioning, level of inspiration) Good positioning: Frontal: Spinous process centered between the medial ends of the clavicles Lateral: ribs superimposed, sternum has minimal thickness Film quality: Frontal: marking noted in lungs, vertebrae visible through heart Lateral: visualize both lungs, adequate spinous penetration Level of inspiration: Sufficient: at least 10 posterior ribs above diaphragm (adult) Insufficient: heart is enlarged, lungs appear dense
Management: Eval decisions: fever
If obvious cause for fever by H and P, no further testing. If no obvious cause, H and P should guide evaluation. - E.g. erythematous throat- check for streptococcus by throat swab. Bloody diarrhea- stool culture. CBC and blood cultures if a child is ill-appearing with signs of sepsis. If neck stiffness or other signs of meningitis, or neonate- lumbar puncture. More extensive work-up if neonate, comorbid conditions, immunodeficiency. *** In severely ill infant/child, one may need to administer antimicrobials prior to evaluation.
Transcytosis
IgD is not secreted, and IgG and IgE are only secreted as monomers, IgA and IgM can form polymers with the assistance of the J chain polypeptide. In order for IgA to provide any protective function it must be transported across the epithelium The basal side of epithelial cells in the gastrointestinal tract, the respiratory tract, tear ducts, and mammary glands express the poly Ig receptor which is responsible for binding to the J chain and activating transcytosis. On the apical side of the cell, an enzyme cleaves the poly Ig receptor, releasing the secretory component (a small portion of the poly Ig receptor component responsible for increasing the antibody half- life), which remains attached to the polymeric IgA or IgM into the mucus, tears, or breast milk on the luminal side.
MISCELLANEOUS/RARE CAUSES
Impaired coagulation Pulmonary endometriosis 3.
1. Define and classify respiratory failure
Impaired gas exchange defined as PaO2 <60 = hypoxemia PaCO2 > 50 = hypercarbia
State the origin of atmospheric pressure (Patm).
In 1643, Thorricelli
Hygiene hypothesis:
Increased exposure to pathogens early in life decreases the likelihood of developing allergies. Supporting evidence - children are less likely to develop allergies if: they are in daycare they have multiple siblings live in developing nations they eat dirt
Massive Hemoptysis Triaging the Causes
Infection: Tuberculosis, aspergilloma/mycetoma, lung abscess Malignant: Endobronchial vs. Parenchymal Inflammatory: Bronchiectasis,sarcoid VascularAnomalies: AVmalformation, aortobronchial fistulas, tracheo-innominate fistula, Kaposi sarcoma Antifibrinolytic drugs that competitively inhibit the conversion of plasminogen to plasmin thereby hindering fibrinolysis. Inhaled tranexamic acid is now being used for hemoptysis treatment in cystic fibrosis.
Etiology in infant/child: fever
Infectious Inflammatory Neoplastic Miscellaneous
Recognize how certain types of lung infiltrates can predict a possible infectious cause
Infectious Bacterial: S. aureus, GNB, Legionella, Nocardia Viral: CMV, Herpes simplex, Adenovirus, Varicella-zoster Fungal : Cryptococcus, Aspergillus, Mucormycosis, Candida Mycobacterial:M. tuberculosis, Atypical Mycobacteria Parasitic: Pneumocystis, Strongyloides, Toxoplasma Noninfectious: Pulmonary edema,Cytotoxic drug-induced lung injury,Radiation pneumonitis/fibrosis,Leukostasis,Leukoagglutinin reaction,Spread of underlying neoplasm, Leukemic cell lysis, Pulmonary hemorrhage
Main differential hilar Adenopathy
Infectious including fungal and TB Lymphoma Sarcoidosis Metastasis
Discuss the major components of the immune system and their role in the immune response. 1° Lymphoid organs:
Innate and Adaptive immune cell production Bone marrow (red)—> Hematopoiesis, B and T cell production BUT only B cell dev Thymus—> T cell Dev Liver (fetus)—> Hematopoiesis (later in the bone marrow)
Transposable Elements
Insertion sequences (IS) - encode enzymes for site specific recombination, mediate own insertion/duplication, leaves behind original copy Transposons - same as IS but larger and code for Ab resistance
Physical:
Inspection: Symmetry of bony thorax and soft tissues Structural deformities Scar formation Rate, amplitude, and rhythm of respiration Kussmaul respirations Cheyne Stokes respirations Palpation: Increased muscle tension Point tenderness Restriction of motion Tactile fremitus
Chronic Sinusitis
Irreversible mucosal thickening In severe long-lasting cases, bony thickening of sinus walls
Other Neurogenic Reflexes
Irritant receptors in the upper airway are stimulated by deformation, dust, smoke, or toxic gases. Afferent signals from irritant receptors are transmitted via the vagus, trigeminal, or olfactory nerve to the integrator to initiate coughing or sneezing. The arterial baroreceptors (carotid sinus and aortic arch) can reflexly alter breathing rate. A reduction in arterial blood pressure stimulates breathing, while a rise in bp decreases it. stretch or proprioceptors located in skeletal muscles, tendons, and joints. When stimulated by movement, these receptors increase ventilation. stimulate the increase in ventilation associated with exercise and help in adjusting ventilation to the external workload. the arterial chemoreceptors are the most important sensors in regulating ventilation according to the metabolic needs for O2 uptake and CO2 excretion.
Obstruction VS Restriction: Obstruction—>
Issue is with exhaling (Vout). So we will see on spirometry a normal inhalation (Vin) BUT a delayed exhalation. (obstructed) FEV3=FEV1 (normal). On the Flow-Volume loop, There will be a shift to the left because less volume is exhaled BUT there is a normal inspiration.
Restrictive—>
Issue with inhaling (Vin). So we will see on spirometry a decreased inhalation and a decreased Vout because less Vin. On the F/V loop, there will be a shift tot the right. Chapter 7 - Gas Transport: Lungs and Periphery
6. Explain how the introduction of air, fluid, or blood could impact the volume of the pleural cavity and consequently that of the lung.
It can restrict the volume in which the lung can expand
Explain the physiologic response of inflammation
It is a local response to an insult (burn, trauma, infection etc.) Cytokines are released → major players: IL-1, IL-6, IFN-gamma, TNF-alpha Local changes due to cytokines: ↑ local blood supply to inflamed tissue ↑ permeability of blood vessels, allowing clotting factors & neutrophils to leak into the surrounding tissue. Disruption of laminar flow of blood pushes neutrophils which usually travel in the center of the blood vessel to the margins so that they can leak through. Elicit pain response Anti-inflammatory mediators then "put out the fire and clean up the battleground" once the insult has been defeated Problem occurs when the insult/trauma continues despite the local response (ex. Bacteria proliferate faster than the inflammatory response can keep up with) → body responds by increasing the inflammatory response, which can progress to a systemic level where the cytokines Systemic changes due to cytokines (act on the hypothalamus): ↑ Basal metabolic rate = fever ↑ HR + ↑ RR = ↑ blood flow to affected regions Systemically marginate more leukocytes
Understand how cytokines participate in host defenses Cytokines Important role in lung innate immunity TNF-α
LPS potent stimulus of TNF-α TNF-α stimulates AM to produce IFN-γ to stimulate more cytokines Increase local levels in lung reduce bacterial counts and increase survival Increase systematically may worsen survival
How to systemic view films:
Large airways → Hila → Bronchi → Diaphragm → Soft tissues
Side Effects:
Lecture 2 (session 2): Micro- Bacterial Classification/Structure
Lecture 19 week 2: Hilar anatomy and pathology
Left hilum more superior than the right Left pulmonary artery passes over left upper lobe bronchus Right pulmonary artery passes horizontally across mediastinum Left pulmonary artery is superior to right pulmonary artery Azygos vein passes over right upper lobe bronchus to join superior vena cava
X-ray in sinusitis
Limited To determine whether or not air fluid level is present Inadequate anatomic detail Cannot precisely define location and extent of disease or cause of disease.
3. Periplasm (G- bacteria only)
Lipopolysaccharide (LPS) = endotoxin Triggers inflammatory response --- shock or DIC Major virulence factor for G- leading to sepsis LPS Lipid A = toxic component Core polysaccharide O antigen = makes it look smooth LOS = always lacking O-antigen bacteria (Neisseria, H. flu)
Part 2: Antibiotic Treatment of Lower Respiratory Tract Infections: Bacteria pneumonia Comprehend radiologic features.
Lobar consolidation Patchy consolidation (more in radiology lectures)
Positron Emission Tomography (PET)
Looks at physiology Finds metabolically active tissue Evaluates for malignant and inflammatory tissue No patient motion b/w CT/PET scans
Bronchial:
Loud and high pitched Distinct pause between inspiration and expiration Expiration is longer, harsher, and higher pitched than inspiration
Tracheal
Loud over trachea Equal inspiration and expiration
Auscultation (breath sounds): Vesicular:
Low in pitch, soft rustling character Actual ratio of inspiration/expiration is 5:6 Audible ratio of inspiration/expiration is 5:1
Overview of transition of respiratory system during birth Stages of development
Lung bud: embryonic, 3-6 wks Bronchial tubules: psuedoglandular, 6-16 wks Acinar tubules: canalicular, 16-26 wks, see some secretory/ciliated cells Terminal saccules: saccular, 26-36 wks, vessels, ciliated cells Alveoli: alveolar, 36 wks to adolescence
Not a obj but heres a list of immunodef states
Lymphoma, leukemia Other malignancies and associated chemotherapy Organ transplants and associated immunosuppressive therapy Neutropenia Immunosuppressive drugs - Steroids Other immunocompromised states Hypogammaglobulinemia,Collagen-Vascular,Asplenia,AIDS
2. Cell Wall (peptidoglycan)
Made up of peptidoglycan Thicker in G+ vs thin in G- G+ also have teichoic acid and lipoteichoic acid G- have an outer membrane LPS/LOS Only in prokaryotes Anti-phagocytic, mitogenic, and/or pyrogenic Blocked by various antibiotics
Chemokines (Not in CP) Interferon-gamma (IFN-γ) ; (Not in CP) G-CSF
Maintain increase neutrophil delivery Increase neutrophil function Enhance clearance of bacteria and virulence faction Non-neutrophil mediated effects Antibiotic interactions Increase levels of certain antibiotics into neutrophiles
Contents of eosinophil granules include:
Major Basic Protein - induces mast cell degranulation; digests sulfated proteoglycans and other connective tissue components, parasite cuticles, the "shell" around parasite eggs, protozoa cysts, and fungal cell walls Acid phosphatase, elastase - degrade tissues such as the thick epidermis of helminthes, yeast, and fungi Eosinophil peroxidase (EPO) - catalyst of eosinophilic respiratory burst Eosinophilic cationic proteins (ribonucleases) - digest RNA, ribosomes (anti-viral)
UROGENITAL:
Male—> Usually sterile except last 1-2cm // Anterior urethra (CNS, Strep and lactobacillus) FEMALE: Urinary tract, cervix and uterus—> Sterile Vaginal tract: change w/ hormonal levels Pre-menarche and post-menarche—> scanty flora (skin and colon) made of Staph, Strep, enterococci and enterobacteriacee Estrogen production—> glycogen support growth of lactobacilli that produce lactic acid decreasing pH—> Lactobacillus, CNS, Strep (group B), Gardenerella mycoplasma, ureaplasma, clostridium, enterococcus.
1-3 month old infants fever
Management depends if the infant is high or low risk. Ill appearing/toxic infants require the same management as neonates. Infants are at low risk if they appear well, have normal physical examination, have a caretaker reachable by telephone, and reassuring laboratory tests. Reassuring labs include: Peripheral white blood cell (WBC) count of 5,000-15,000 cells/μL, An absolute band count of <1,500 cells/μL, Normal urinalysis and negative culture (blood and urine) The negative predictive value with 95% confidence of these criteria for any serious bacterial infection is >98% and for bacteremia is >99%.
SMALL INTESTINE:
Many microbes Increase microbes the farther from the stomach Anaerobes—> Enterococci, peptostrptococci, Porphyromonas, Prevotella)
ERV—>
Max amount of air that can be exhale after a normal tidal volume expiration.
Inspiratory Reserve Volume (IRV)—>
Max amount of air that can be inhale after a normal tidal volume inspiration.
VAP = ventilator acquired pneumonia
Mechanical ventilation increases the risk of pneumonia by 6-21x Occurs in 10% of pts on ventilation Actineobacter (specific to VAP)
CMV
Micro: DNA virsue, herpesvirus group Epi/PG: 1% of live-born infants infected in utero; most common congenital viral infection. Transmission to infant can occur: In utero: transplacentally. Passage through infected genital tract. Postnatally through ingesting milk (doesn't usually result in clinical illness). Fetal risk: most pronounced during 1st half of gestation.
HSV
Micro: enveloped DS-DNA, est latency and reactivation EPi/PG Tranmission: Delivery from mother Genital tract, ascending infx, intrauterine(rare)
Deletions/insertions
Micro: frame shift (not in sets of 3s), changes in gene product Large: due to IS elements or transposons, disruptions lead to non-functional proteins
Congential rubella
Micro:Enveloped, RNA virus. Togaviridae family. Epi/PG: Persistent/Progressive infection Pathology result primarily of virus-induced necrotizing vasculitis Fetal infection can result in miscarriage, spontaneous abortion, or stillborn. -Fetal infection rate: 1st trimester: 80-100% 6 weeks: infection rate drops 10-20% >30 weeks: 60% or higher Cell-mediation= Responses decreased as compared to those after acquired infection; lowest in infants born prematurely. Humoral= Fetal IgM as early as 20 wks/decline by 6 mos; Fetal IgG detected by mid-2nd trimester/ persist for many years
6. Flagella and pili/fimbria
Mobility and help with virulence
IgG and IgM
Most effective opsonizer (IgG) Agglutination of particulate antigens Initiate complement cascade Neutralize or lyse bacteria, viruses
1. Know sterile sites of the human body that are generally devoid of normal microbiota. (BOLD—> ABSOLUTELY Sterile)
Newborn begin life sterile, colonized soon after birth. CNS and Meninges* Cardiovascular system (blood)* Hematopoietic-lymphoreticular system* Peritoneum* Stomach, Digestive glands, pancreas, gall bladder Pleura, lower respiratory tract Kidneys, urinary system, male genital Skeleton and skeletal muscles.
4. Describe the functional interactions between the brain stem centers in generating signals to initiate respiratory muscle activity. Neural interconnections
Most medullary neurons that discharge in synchrony with either inspiration or expiration located primarily in two areas, dorsal respiratory group (DRG) and ventral respiratory group (VRG). Motor neurons from the medullary inspiratory neuron pool initiate contraction of the inspiratory muscles (i.e., diaphragm and external intercostals). Medullary inspiratory neurons diminish activity of expiratory neuron pools in the medulla while facilitating activity of neurons in the pneumotaxic center. As the lung inflates, stretch receptors in the lung are stimulated. Activation receptors enhanced center activity and inhibit the apneustic center. This diminishes of stretch along with pneumotaxic center The rhythmicity of breathing, originating from the brain stem centers, can be voluntarily overridden by input from higher cortical centers. the brain stem centers will eventually dominate the breathing pattern as dictated by the need for CO2, removal or O2 uptake, or acid-base balance of extracellular fluids. Output from the brain stem integrator descends the spinal cord and exits via motor neurons to innervate the diaphragm, intercostal, and abdominal muscles. The diaphragm is innervated by the phrenic nerve formed by C3 to C6. The external intercostals are innervated by the intercostal nerves T1 to T12. The respiratory muscles most important to expiration are the internal intercostals and the abdominal muscles, which are innervated by nerve fibers originating at T1 through T11 and T4 to L3, respectively.
. Review basic prokaryotic cell structural components: A. Cytoplasmic components
Most metabolic rxn take place here Contain ribosomes and protein synthesis machinery Nucleoid -- circular double stranded DNA, supercoid by gyrase plasmids
Understand how the polymorphonuclear cell protects the lung and against which pathogens
Most numerous and important defense once full-blown inflammatory response occurs Sequestered in interstitial areas and capillaries Adherence to endothelium Chemotactic attraction to inflamed site Diapedesis into tissue Ingestion and destruction of microbes Defects take the form of: Absolute deficiency Decreased PMN adherence: Ethanol, steroids, anti-inflammatory agents Decreased PMN chemotaxis : Deficiency of actin-myosin Intrinsic defect Unable to digest organisms (chronic granulomatous disease) Lecture 7 week 2: Pulmonary infections in the immunocompromised
11. Specify the venous angle to which lymph from the following lobes typically drain: any R.lung lobe; L inferior lung lobe, L. superior lung lobe.
Most of the lung will actually go to ipsilateral side. On the left: left upper lobe goes to left venous angle but the lower lobe typically tracks up and follows the lymph from the right. All of the lymph nodes are connected and don't have effective valves making lymph flow pressure dependent. So any one of the lobes can flow into either venous angle
List the principal factors that contribute to the work of breathing and how they are affected by a reduction in lung compliance, increased tidal volume, or breathing frequency,
Most of the work of normal breathing is done during inspiration to overcome elastic recoil of the lungs. In addition, during inspiration work must be done to overcome frictional resistance in airways, as well as a very small amount of viscous resistance in rearranging lung tissue as the lungs inflate. During expiration, the relatively small amount of resistance of airways and tissues is more than taken care of by the natural elastic recoil of the lungs: thus, quiet expiration is essentially a passive process not requiring any additional work input by the respiratory muscles. Chapter 4 - Pulmonary Ventilation
FEV1: Forced Expiratory Volume in 1 second
Most reproducible, most useful measurement Test potency of large airways Ex of diseases: Chronic bronchitis, emphysema, asthma
Apply the SOFA and qSOFA scoring systems
Movement to define sepsis as life-threatening organ dysfunction caused by a dysregulated host response - key thing here is organ dysfunction! SOFA: Sequential Organ Failure Assessment describes organ failure in a continuous form criteria indicating end organ dysfunction: score of two or more + source of infection = sepsis qSOFA: quick-SOFA 3 criteria: score of 2 or more in patients w/infection = ↑mortality Drawbacks of SOFA and qSOFA is that they do not identify early sepsis nor can they be used to guide treatment → thus scoring system for sepsis is still an evolving process Lecture 14 week 2: Pathology of Acute/Subacute Pulmonary infections:
CELL WALL-LESS BACT:
Mycoplasmataceae—> NO peptidoglycan cell wall, pleiomorphic// M.pneumoniae, ureaplasma urealyticum
State the percentages of O2 and CO2 in normal, dry atmospheric air.
N2= 78%; O2=21%, Ar= 1%, CO2= very miniscule (I think)
5) Describe how the appearance of the costophrenic angle might change on an upright x-ray due to fluid accumulation in the recess.
NOT IN LECTURE!! I think the angle should be more pronounce since there is more fluid. Should be blunted see next lecture.
2) Specify the surface location of the inferior margins of the lungs during quiet breathing.
NOT MENTIONED!! Anteriorly—> expiration 6-8 ribs / inspiration 8-10 Posteriorly—> expiration 10 rib / Inspiration 11-12
Supplemental O2:
Nasal cannula: increases FiO2 by 4% for each L/min, 4L should be max Simple O2 mask: gives FiO2 up to 60% Nonrebreather can provide up to 95% O2
Clinical findings of congential infx
Nervous: microcephaly, mental subnoramality, cerebral palsies, seizures, cataracts, micropthalmia, sensorinueral deafness, etc Extraneural: failure to thrive, low gestational birth wght, prematurity, purpura, jaundice, hepatosplenomegaly (HSM), congenital heart disease, etc
Recognize how antibody-mediated immunity protects the lung and against which pathogens IgA
Neutralize respiratory viruses, exotoxins Agglutinate microbial organism for mucociliary escalator Prevent bacterial attachment to epithelial cells
3. Neutrophils
Neutrophils extravasate out of blood vessels and enter surrounding connective tissues to eliminate invading bacteria. contain granules that assist in the destruction of the bacteria. release ROS as they migrate through tissues, leaving behind tissue damage the ROS produced in phagolysosomes of neutrophils is lethal for both the phagocytosed pathogens AND for the neutrophils. This leads to the formation of pus (dead pathogens + dead neutrophils).
Granulocytes: Mostly innate immunity
Neutrophil—> phagocytosis and inflammation response Eosinophils—> Phagocytosis large parasites, fungi, helminths and protozoa, inflammation and allergic response. Basophils—> allergies
Adaptive IS:
No physical/chemical barriers Location—> production in bone marrow (B/T cells), development in Bone marrow (B) and in thymus (T cells). Activation in 2° lymphoid organs (both) Function—> very specific to pathogen involved. Involves differentiation of naive cells to effectors cells. Timeline—> 1° response is slow (days-weeks) but 2° response is fast (hours-days)
Mast cells
Non phagocytic fixed cells w/in lamina propria and submucosa of respiratory and digestive systems, serous membranes, mesentery, dermal papillary layer, and the hypodermis.
FEV1/FVC Ratio
Normal value typically 75-85%, decreases with aging Less than 70% indication of obstruction Can quickly identify persons with airway obstruction where the FVC is reduced Valuable for identifying the cause of low FEV1 Ex. of disease w/↓FEV1 and ↓FEV1/FVC ratio: COPD (chronic bronchitis, emphysema), asthma, bronchiectasis
Understand the various components of a pulmonary function test and their indication
Normal values for lung volume and flow rate are based on: age, sex, height and race. WEIGHT not included!
12. List the structures of the mediastinum and root of the neck that are at risk of compression from a Pancoast tumor or enlarged hilar lymph nodes.
Not in lecture Chapter 1 - Histology Chapter 2 - Basic Concepts
Transient tachypnea (TTN) Tx/Clinical Course (CC):
O2, may restrict fluid(not diuretics) , resolves in 3-4 days (if not improving in 24 hrs consider alt Dx) , higher risk of wheezing
DX: HSV
Obtain following: Swabs of morth, nasopharynx, conjunctivae, anus, or skin vesicles for culture or PCR CSF and Blood-PCR Typing can differentaite 1 or 2 Tx: Acyclovir IV 14 days (Sem disease) or 21 day (CNS or dissem dis) Following that 6 mos of oral acyclovir for suppresive, eye exam, nueroimaging, and Lumbar puncture at end of tx with CNS invovle Ask about HSV in women/partner Suppressive antivirals for active infection for mothers at 36 weeks A lot of more guidelines in CP
Predisposing conditions leading to HAP
Old age Prior surgery Ventilator therapy Serious underlying disease, often of the lungs Due to Legionella Cytotoxic chemotherapy Corticosteroid use
Describe how surfactants enhance alveolar stability and reduces the opening pressure of collapsed alveoli,
On #10
Hx: must be thorough fever
Onset Other symptoms Exposures (daycare, school, family, pets, playmates) Travel Medications Other underlying disorders Immunizations HPI: Exact age Temp and how it was taken Duration of fever Pattern of fever Thorough ROS Sick contacts Travel Pets Daycare Meds given PMH: Prior abx Comorbid conditions Prior hospitalizations and surgeries BirthHx: Gest. age Mode of delivery Pregnancy problems and perinatal complications ***Especially important in infants!!! Immunization status FH DEV HX.
Transient tachypnea (TTN) CP:
Onset w/in 2 hrs of delivery Tachypnea (>60bpm) , more breathing work, nasal flaring, clear breath sounds
Neisseria—>
Oxidase + and usually commensal
X‐ray Views
PA - beam goes thru pt from posterior to anterior AP - beam goes thru pt from anterior to posterior Used when pt needs to be seated b/c heart looks enlarged, lungs not as expanded. ex.) supine/portable x-ray -- for very ill pts -- uses AP view Lateral - confirms PA and AP views Decubitus - pts lays on the left side Good for accessing free vs loculated fluid in pleural effusion Lordotic - looks at the lung apices
Calc A-a gradient:
PAO2 = (0.21 * 760) - (75 * 1.25) = 72 Given PaO2 is 45 so 72-45 = 27 50 y/o M so gradient should be less than 50/4 + 4 = 16.5 Note: if give O2 you can possibly knock out pt hypoxemic drive, making acidosis worse Oxygen Transport and Delivery Respiratory Failure
Viral infxs of Fetus/newborn: general
PG: inoculation of mucosal surface→ local replic→ primary viremia→ 2ndary replic→ 2ndary viremia and dissemination Viral infx of fetus generally follows mother or placenta replic Earlier in utero normaly worst bc of low immune maturity
GRAM - Cocci:
PINK on gram stain
Pneumothorax
PP: air leak from alveoli, air gets into space between pleural and visceral layers Squished lung → atelectasis → V/Q mismatch, can decrease CO and cause shock RF: premature, ventilation, meconium aspiration syndrome, pna, TTN CP: Resp distress, grunting, pallor, cyanosis, chest asymmetry CXR: flat diaphragm, mediastinum shift away from pneumo, atelectasias Tx: can resolve 1-2 days and watch closely for infants w/o air leak or resp distress, O2, minimize airway pressure if ventilated Thoracentesis for symptomatic Tension pneumothorax and pneumothorax in a mechanically ventilated infant require a chest tube
Diaphragmatic hernia:
PP: abd contents squeeze into thorax Can cause pulm hypoplasia, Can see pulm HTN CP: see resp distress at birth and scaphoid abd Tx: intubation, NG tube for decompressing stomach, ECMO maybe, Surgical repair when stable
Congenital pulmonary airway malformation (CPAM):
PP: Congenital malformations cause cysts in lung parenchyma Caused by Abnormal branching → infections, air trapping, possible malignancy TX: All infants should have CT or MRI Require resection if high risk or symptomatic Large lesions, bilateral/multifocal cysts, FH of pleuropulmonary blastoma-associated conditions, or pneumothorax Lecture 1 (session 2): Pharmacology of Bacterial Infections
Meconium aspiration syndrome:
PP: aspiration of meconium thick, black debris from intestine Sterile, color comes from bile Passage uncommon after 20 wks but can be due to fetal distress Aspirated during fetal gasping or first breaths after delivery Causes pulmonary disease airway obstruction Causes atelectasis and air trapping Inflammation Exudative and inflammatory pneumonitis with epithelial damage and alveolar collapse surfactant inactivation Related to increase surfactant inhibitors RF: long gestation, African/South Asian, breech delivery CP: Meconium stained fluid, birth depression, resp distress/cyanosis(immediate) , crackles, pneumothorax common May have resp failure, associated w/ pulm HTN of newborn Tx/CC: resp support, ABx & culture to prevent pna, surfactant therapy if intubated, echo if resp distress is severe May have prolonged hospital stay, wheezing in 1st 6 mo of life,
Pulmonary hypoplasia:
PP: incomplete growth of lung Due to renal agenesis, amniotic fluid leak, skeletal abnormalities, pts w/ oligohydramnios have worst outcome Less fluid, worse prognosis, high mortality CP: severe resp distress at birth Tx is supportive to allow lungs to grow
Tracheoesophageal fistula (TEF)
PP: often w/ esophageal atresia Prenatally often have polyhydramnios CP: Present with excessive oral secretions and inability to feed H-Type TEFs may present with coughing and choking with feeds Dx :when they can't pass catheter into stomach TX:Requires surgical repair Post-repair complications are common - Tracheomalacia, motility disorders, esophageal stricture
Bronchopneumonia
PP: Organisms and inflammation spreads along airways (bronchioles and bronchi) Neutrophils fill airways and then extend into adjacent alveoli (patchy consolidation) Involved areas may coalesce and appear like a lobar pneumonia May be a pattern seen with viral etiologies or aspiration
Lobar pneumonia
PP: org and inflammation spread through pores of Kohn=interalveolar connections) Neutrophils fill alveoli→ solidify large region/lobe = consolidation Consolidated lung is heavy/solid feeling (takes appearance of the liver Red hepatization = earlier, consist of pus, neutrophils, edema, red cells/congestion and some fibrin Grey hepatization= later, consists of broken down red cells, >macrophages and fibrin, and some fibroblast for fibrosis
Physiological factors can alter airway resistance
PSNS (Ach) Bronchoconstriction of airway smooth muscle Increases mucous secretions → increasing airway resistance SNS B2 adrenergic receptors -- Promote bronchodilation by relaxing airway smooth muscle. Limits secretions via vasoconstriction CO2 Decrease airway CO2 = bronchoconstriction Increases in airway CO2 = bronchodilation
6. List specific characteristics and/or diagnostic tests that would allow you to differentiate between the classes of bacteria. GRAM + COCCI:
PURPLE on gram stain
Define partial pressure of a gas in a gas mixture.
Partial pressure=Pg= is the fraction of the gas (Fg) in the mixture=(Fg)(PB)
6. Using examples, explain the similarities and differences between PAMPs and PRRs (pathogens, cells, locations) as well as potential consequences of these receptor-ligand interactions. PAMPS
Pathogen associated molecular patterns: LPS, peptidoglycan, dsRNA, teichoic acid, and flagellin Can be on bacteria viruses, fungi, protozoa. Not on human cells Recognized by host cells or plasma proteins: Therapeutic targets
14.Explain the innate and adaptive immune system defects affecting the respiratory system (TLR deficiency, chronic granulomatous disease, Bruton's agammaglobulinemia, and selective IgA deficiency). Toll like receptor (TLR) deficiency:
Patients have an increased susceptibility to Gram positive bacterial infections, Streptococcus pneumoniae meningitis. Defects in TLR signaling pathway (X linked mutations of NFĸB documented) can result in: Inappropriate activation of inflammation → autoimmune arthritis, asthma, septic shock, lung fibrosis, atherosclerosis Persistent inhibition of activation → recurrent skin infections in infancy, recurrent respiratory tract infections, diarrhea, failure to thrive (FTT)
Macrophages—>
Phagocytosis, APC, repair and release cytokine to activate other immune cells.
Lower Respiratory Tract (Terminal bronchi and alveoli) defenses
Phospholipid surfactant Proteins (immunoglobulins, complement) Cellular defenses Lymphocytes Alveolar macrophages Polymorphonuclear Neutrophils
2. Contrast the innate and adaptive immune systems in respect to their immune components (physical barriers, chemical barriers, cells, and molecules), the location of production and functions of these immune components, and timeline involved during an immune response. INNATE IS:
Physical and chemical barrier—> see below Location—> produced and developed in the bone marrow during hematopoiesis Function—> Non-Specific and therefore, same response to any pathogen. PRR (on IS) binds to PAMPS (on pathogen) to initiate response. Timeline— relatively fast (1-12hrs)
Poiseuille's law
Poiseuille's law takes into account the physical dimensions of the tube (radius and length) and the nature of the fluid moving through the tube. Poiseuille's equation states that frictional resistance to flow is directly related to viscosity of the fluid and the length of the tube and indirectly related to the fourth power of the tube radius (r4). Limitation → However, lung airways are distensible, compressible, and not perfectly round or smooth. Furthermore, lung airways branch repeatedly and exhibit changes in radius and length during each breath. Poiseuille's equation also does not compensate for changes in the airflow pattern such as from laminar to turbulent, where frictional resistance is higher.
Physiologic dead space—>
Portion of the tidal breath not involved in gas exchange (comprise the anatomic and the alveolar dead space)
Massive Hemoptysis Initial Approach
Position patient Bleeding side down Airway protection: Endotracheal intubation IV access for Volume resuscitation ICU transfer If hemodynamic and respiratory compromise Rigid bronch or Large endotracheal intubation and FOB Consultation Interventional radiology Interventional pulmonary thoracic surgery
Dx Taxoplasmosis
Prenatal: DNA (amniotic or blood), culture, serial Ultrasound Postnatal: Serum serology of mom and baby Tx: Prior to 17 weeks gestation: Spiramycin (does not treat fetus if infection has spread to placenta) After 17 weeks:Pyrimethamine and Sulfadiazine and folinic acid Infant: same as after 17 weeks, steriods if CSF protein high Prevention: avoid cat poop
Dx: CMV
Prenatal: PCR amniotic fluid After birth: PCR bodily fluids; CMV IgM serology not very reliable TX: Neonates with symptomatic give either oral valganciclovir or IV gnaciclovir for 1st 6 mos of life (improves hearing and nuerodev) Side effects: Neutropenia and LFT elevation
List the three physical factors that determine the pressure exerted by a gas.
Pressure= (n/v)RT R is the ideal gas constant n = number of gas molecules in the container (usually measured in moles) V = volume of the container (usually measured in liters) T = temperature of the gas (usually measured in degrees Kelvin)
2. Describe the various etiologies of respiratory failure
Pump failure → hypercapnia = high CO2 Lung failure → hypoxemia = low O2
TX: respiratory distress
Prevent w/ antenatal steroids, accelerate cell development Best for babies born 1-7 days after steroids CPAP, intubate and give surfactant if that doesn't work, caffeine NIPPV is (+) pressure without intubation Intubation and Mechanical Ventilation Indicated for patients who fail to respond to less invasive forms of ventilation Minimizing volutrauma, barotrauma and oxygen toxicity Permissive hypercarbia Target oxygen saturations in the low 90's Surfactant Administer to those requiring intubation - Most effective when given within the first 30-60 minutes of life CC: Prolonged hospitalization, bronchopulm dysplasia (BPD), developmental delay
Recognize how alveolar macrophages protect the lung and against which pathogens
Primary Defense: Phagocytic against various antigens Secondary Defense Modulation of function of other inflammatory and immune responses Presentation of processed antigen to T lymphocytes • Complement fragments Chemotactic factors to PMN Lymphocyte chemotaxin Leukotrienes Intracellular Microbes Contained by Macrophages Mycobacterium tuberculosis Mycobacterium lepraemurium Toxoplasma gondii Leishmania donovani Legionella pneumophila Pneumocystis jiroveci Listeria monocytogenes Cytomegalovirus HIV
Dendritic cells—>
Professional APC for both intra/extracellular pathogen. Present MHCI and MHC II to T cells. Can cross present to B and T cells.
Recognize how complement system protects the lung
Properdin Factor B Direct lysis Opsonization Defects: C3 and C5 deficiency Potential infectious problem: Non life-threatening infection
G- AEROBIC RODS:
Pseudomonas—> non-fermenting, oxidase+, cat+ / P.aeruginosa and Burkholderia cepacia (opportunistic) Legionella—> L.pneumophila (legionnaire disease and Pontiac fever) G- aerobic coccobacilli—> Bordetella, fransicella, brucella.
J-Receptor Reflex
Pulm juxtapulmonary-capillary receptors, are located in/near, the walls of pulm microvessels. stimulated by vascular emboli, interstitial edema and chemicals (phenyldiguanide or capsaicin). Information from the J-receptors is delivered via vagal afferents in the brain stem. stimulation results in rapid shallow breathing (tachypnea). responsible for the psychological sensation of "air hunger", (dyspnea.)
Extra
Pulmonary Function Tests
VASCULAR DISEASE
Pulmonary embolism Elevated pulmonary venous pressure Left ventricular failure Mitral stenosis Vascular malformation
PE: Chest exam
Rales audibles before infiltrate Localized wheezes suggest endobronchial lesion Pleural friction rub with pulmonary infiltrate suggests virulent GNB or fungus Respiratory rate sensitive of severity
Fiberoptic Bronchoscopy
Recommended : Central diffuse or focal lesions, No specimen by sputum or transtracheal, No response to antibiotic therapy Complications hemorrhage or pneumothorax (7%)
Open lung biospy
Recommended: Diffuse or focal infiltrates, Where other techniques have failed or given nonspecific diagnosis Complications: Pneumothorax 8%, Bleeding (rare),Mortality 0.6%
Aspiration lung biopsy
Recommended: Focal, peripheral lung infiltrates;Fluoro directed aspirations: 70-90% accurate;64% false negative rate Contraindicated: Inadequate platelets or coagulation, Uncooperative patient, Bullous emphysema Complications: Pneumothorax 25% ,Self-limited hemoptysis 2-5%, Local bleeding at site 11%
NON-SPORE_FORMING G+ RODS:
Regular shape—> Listeria monocytogenes (meningitis and bacteremia in neonates and immunocompromised) Irregular—> Corynebacterium diphtheria
DX: rubella
Req virlogic or sero Viral: RT-PCR/genotyping from blood, urine, catract,throat,nasal Serology (often gives false results) Tx: supportive Prevention: if pregant mother not immune wait until baby is born Active Immunity: Live Vaccine- 2 doses generally given at 12-15 months and 4-6 yrs alone or as MMR Passive Immunity: Immune Globulin
2. Know which sites of the human body generally have specific normal microbiota. (FOCUS ON BOLDED MICROORGS!! I DON'T THINK WE NEED TO KNOW ALL THIS) ONLY FOCUS ON "RED" IF NOT ENOUGH TIME (look #7) SKIN:
Resident—> Coagulase-negative Staph (S.epi), Proprionibacterium (acnes), Micrococcus and Acinetobacter (G-) Transient—> Corynebact, S. Aureus, Strep, Clostridium (perfringens) and Bacillus. Less G- b/c skin too dry + salty sweat.
Adventitious:
Rhonchi Sibilant Sonorous Rales (Crackles) Crepitant Subcrepitant Bubbling Voice sounds: Whispered pectoriloquy Egophony Bronchophony
G- OBLIGATE INTRACELLULAR:
Rickettsiaceae—> zoonotic w/ arthropod vectors // R.rickettsia, R.prowazekii, R.typhi, Coxiella chaffeensis, Ehrlichia ewingii Chlamydophila psittaci
11) List the factors that cause a shift in the oxyhemoglobin dissociation curve and their effect upon affinity of O2 for Hb and O2 delivery to the tissue.
Right shift—> Decrease affinity, increase unloading (delivery). VICE-VERSA!!! High CO2 and Low pH Bohr effect—> Binding of CO2 or H+ to Hb decrease its affinity to O2 which is therefore unloaded. High T°C High 2,3-DPG High in anaerobic or hypoxic cdts Left shift—> Opposite of above high MetHb High CO
I. Review basic prokaryotic classification: A. Morphologically
Rods, coccus, helical rod (spirochete) Pleomorphic -- varies in size and shape Cell arrangement: pairs, chains, clusters
Know the role and how to interpret the diffusion capacity in lung disease
Role: estimates transfer of oxygen from alveolar gas to hemoglobin in RBC Dependent on: 1) area of alveolar-capillary membrane 2) Thickness of membrane 3) Driving pressure - difference in oxygen tension between alveolar gas and venous blood Interpretation of results:
Identify the four SIRS criteria
SIRS: Systemic Inflammatory Response Syndrome Need 2 or more of the following for a SIRS diagnosis Leukocytosis: WBC count >12,000 Bandemia: "Left Shift", 10% or greater percentage of bands
Accessory muscles
Scalenes and sternocleidomastoids Minimally active during eupnea Contraction of scalenes elevates the first ribs Sternocleidomastoids raise the sternum Inactive until ventilation reaches 50-100L/min and associated w/ heavy exercise
Local immunoglobulin coating
Secretory IgA major immunoglobulin upper airways Prevent adherence and absorption Antibody activity against viruses, bacteria, allergens Defects IgA deficiency Functional deficiency by bacterial breakdown (protease) Streptococcus pneumoniae, haemophilus influenzae Potential infection problem Sinopulmonary infection Abnormal colonization with certain bacteria
Explain why aerobic multicellular animals, unlike unicellular organisms, require the transport of gases between the atmosphere and tissues.
Seems self explanatory
FVC: Forced Expiratory Vital Capacity
Sensitive to diseases that alter mechanical properties Tests the expansion of chest wall and lungs Ex. of restrictive diseases: interstitial lung disease, pulmonary fibrosis, chest burn scars, ascites, pregnancy obesity Ex. of obstructive diseases: COPD, asthma
Differentiate between systemic inflammation and sepsis
Sepsis: 2 or more SIRS criteria + a source of infection Common causes of infection: pneumonia (47%), Intra-abdominal processes (18%), UTI (18%), Bloodstream (12%)
6) Given an x-ray of the thorax, be able to identify the regions that represent the lobes of the lungs.
Should be able to do this
7) Given a clinical scenario involving pulmonary signs and symptoms be able to determine the most likely lobar location of the pathology.
Should be able to do this!! Thoracic Cavity and Lungs
Computed Tomography (CT)
Single slice - no longer standard Spiral - fast, decreases motion artifact, IV bolus of contrast material can be followed Multi-detector CT - Can scan even faster than a single detector. Can scan the lung in 30 sec. with 4 slices and 4 sec. with 64 slices. High resolution CT - detail look at lung parenchyma, thinner slices but not contiguous (can miss lesions). Indications for pts w/ signs and symptoms of lung disease but normal CXR and/or thicker standard CT slices. Diffuse infiltrative pulmonary disease on chest x-ray or thicker standard CT slices.
Extrathoracic
Skin: Ecthyma Gangrenosum (pseudomonas, aspergillus), Cutaneous papules (cryptococcus, nocardia) Retinal lesions: CMV, Candidiasis, Aspergillosis Necrotizing nasal lesions: Mucor, Aspergillus, GNB CNS: Meningitis (cryptococcus, tuberculosis, cancer), space occupying (nocardia, mucor, cancer), encephalitis (herpes, toxoplasmosis)
9. Discuss the characteristics of the five major classifications of antibody isotypes and explain their various effector functions in relation to providing immune protection to the host.
Some antibody isotypes (IgG, IgA) have additional subclassifications which perform specific effector functions. For example, some subclassifications of IgG can neutralize whereas others can opsonize and promote phagocytosis. With the exception of IgD, all of the other antibody isotypes can be secreted.
Know the indications, general methodology performance, and interpretation of the routine tests used to evaluate pulmonary function
Spirometry - also refer to LO5 for further interpretations of FVC, FEV1 Flow-Volume Loops - discussed above Diffusion Capacity - discussed above Fractional Exhaled Nitric Oxide: - used to assess allergic/eosinophilic asthma status - simple and safe, good POC tool but expensive - if FeNO is elevated treat with corticosteroids Arterial Blood Gas - according to Dr. Gobel this is the one true pulmonary function test! Immunology
Understand general principles of empirical Tx. Lower Respiratory Tract Infections: Bacteria pneumonia
Start w/ broad-spectrum antibiotic Once culture is ready - treat specific organism (within 48-72 hrs)
STOMACH:
Sterile due to acidic pH Acid resistant G+—> Step, lactobacilli, H.pylori
Define surface tension and describe how surfactants work to alter surface tension,
Surface tension is defined as a manifestation of attracting forces between atoms or molecules. The force of surface tension acts in the plane of the air-liquid boundary to shrink or minimize the liquid-air interface (see figure). However, unlike the flat interface present in the beaker, alveoli are nearly spherical in shape, so surface tension forces of the fluid film lining alveoli must be considered for a sphere. - surface tension increases the likelihood of the alveoli to collapse. Law of LaPlace says P=2 x surface tension/radius Alveolar instability - Tells us that with constant surface tension smaller alveoli radius have higher pressure compared to larger radius alveoli so air would travel to the larger radius alveoli → thus collapsing the smaller radius alveoli.
Fetus and newborn humoral immunity
Surface+ B-lymphocytes in marrow: 22 wks gest. Stimulated B-lymphocytes secrete predominantly IgM: fetus-newborn. Serum IgG reaches 60% of adult level: 1 yr IgG crossed the placenta but IgM doesnt Ab production in response to polysaccharide Ags: 2- 3 yrs. Stimulated B cells secrete all isotypes: 2-5 yrs.
Identify the production site and principal chemical constituents of lung surfactant,
Surfactant made in Type ll alveoli cells Is amphipathic -- Has two sides Hydrophilic - on water side Hydrophobic - on air side
Surfactant
Surfactant naturally accumulates at the liquid-air interface to reduce the number of water molecules that would normally occupy the interface. The presence of surfactant molecules disrupts attracting forces between water molecules to reduce surface tension. As surface area is decreased, such as when an alveolus deflates, the relative concentration of surfactant molecules per unit area tends to increase. As alveoli inflate, water molecules must be brought to the interface, so surface tension increases as fewer surfactant molecules are present per unit area. Basically means: smaller alveoli = more surfactant = decrease ST → decrease P → increase the amount of air it receives Vs. larger alveoli = less surfactant = higher ST → higher P → receives less air The LaPlace relationship is still applicable, however, alveolar surface tension is not constant but decreases as alveolar radius decreases. As a result, pressures in small-radii alveoli are less than in large-radii alveoli.
Pneumonic infiltrate:
Tactile fremitus increased Dullness to percussion Bronchial breath sounds Increased Voice sounds Whispered pectoriloquy Egophony Bronchophony 12. Arterial Blood Gasses (NO LOs, so I just did a summary outline of lec)
Type IV Hypersensitivities:
These immune responses primarily involve helper T cells (Th1 cells and Th17 cells), although cytotoxic T cells (CTLs) and B cells may also be involved in the disease process. This reaction is characterized by a delay in the immune response, typically 24- 72 hours post antigen exposure in an acute response, or after a week as in the case of a chronic response.\
The Blood Brain Barrier
The BBB separating blood from brain tissue is freely permeable to O2 and CO2, but largely impermeable to charged ions, such as H or HCO3 Thus, CO2 present in blood can readily diffuse into the CSF where, in the presence of carbonic anhydrase, it can undergo hydration to form H and HCO3 . the central chemoreceptors are more sensitive to changes in the H+ than the CO2 of CSF. chemoreceptor stimulation depends on the free entry of CO2 into the CSF and subsequent hydration to H . The central chemoreceptors are not sensitive to changes in blood H+ because entry of H+ into the CSF is limited by the BBB
Cerebral Spinal Fluid
The CSF has a lower protein concentration, higher PCO2 and lower pH than arterial blood and lacks hemoglobin (Hb). Because of the lack of Hb and the low protein concentration, CSF has a much lower buffer capacity than blood.
Calculate the pressure of oxygen in the atmosphere, in the airway and in the alveolus Airway
The addition of water vapor to inspired air has to be considered in calculating partial pressures of the other gases present in air. Since the PH2O of saturated air at normal body temperature (37°C) is 47 Torr, it reduces the partial pressure of all the other gases present in the mixture by a proportionate amount.
Stimulation of Peripheral Chemoreceptors
The carotid and aortic bodies are able to monitor the physically dissolved O2 and CO2 and the H+ concentration of arterial blood. These chemoreceptors are stimulated by a drop in PO2, especially below 60 Torr also stimulated by an increase in the arterial blood H+ concentration (decreased pH) or an increase in physically dissolved CO2 (or PCO2). They are the only sensors capable of detecting a fall in the PO2 and account for increases in ventilation resulting from hypoxemia. But they only detect levels of physically dissolved O2 and not the O2 that is chemically attached to hemoglobin.
Carotid and Aortic Bodies
The carotid body is on the bifurcation of the common carotid artery just above the carotid sinus baroreceptors and are more important The aortic bodies are above and below the aortic arch. The peripheral chemoreceptors have a high metabolic rate but also have an exceedingly high blood flow of about 2000 ml/100 g of tissue. As a result, its difficult to detect a PO2 difference between the blood entering and leaving the carotid body. The carotid bodies are comprised of several cell types, but are mostly glomus cells
6. Identify and locate chemoreceptors that monitor extracellular fluid pH, carbon dioxide, and oxygen tension. Chemoreceptor Reflexes
The chemoreceptors are specialized cells capable of detecting changes in the concentration of physically dissolved O2, CO2, or hydrogen ion (H+) in the extracellular fluid surrounding them. These chemosensitive cells are divided functionally, into the peripheral and central chemoreceptors.
State the effect of altitude on the percentage of O2 in dry atmospheric air.
The fractional percentage composition of all gases remains unchanged
Identify the factors responsible for the adherence of the visceral to the parietal pleura,
The intrapleural fluid has cohesive forces/surface tension that help to join or link the visceral and parietal pleura together. As the chest wall expands during inspiration, the lung is obligated to follow, so the two structures expand as a single unit. The intrapleural fluid has water in it and water has surface tension properties. This allows water to stick to other surfaces and also itself more than other liquids.
2. Explain how the anatomy of the right and left main bronchi relate to aspiration.
The left main bronchus departs from the trachea at a greater angle than that of the right main bronchus. The right bronchus is also wider than the left and these differences predispose the right lung to aspirational problems.
Describe the common pneumonic syndromes/presentations, the organisms involved, and the characteristic associated pathologies Community-acquired acute bacterial pneumonias (particularly concepts of lobar pneumonia and bronchopneumonia)
These infxs are acquired by healthy people in the normal environment sometimes as a secondary infx following an URT infx CP: Abrupt signs and sxs High fever, shaking chills, pleuritis/chest pain, Purulent sputum, possibly hemoptysis ('rusty' colored sputum), elev acute phase reactants Determining (by culture or other) the causative agent and the extent of disease is paramount, as it guides appropriate therapy. From a pathology perspective, two broad patterns of disease can be mechanistically described
7. Describe how alterations in pH, carbon dioxide, and oxygen interact to influence or alter ventilation. Contribution of Arterial vs. Central Chemoreceptors
The most potent stimulus to ventilation is an increase in CO2. PCO2 of arterial blood is closely maintained around 40 Torr by the medullary center via chemoreceptor input. the PO2, monitored only by the peripheral arterial chemoreceptors, has to decline markedly (from 100 to 60 Torr) before ventilation is noticeably increased. This would correspond to a decrease in the inspired O2 from 21% to about 8%, The central and peripheral chemoreceptors respond to changes in PCO2 of the CSF and arterial blood, respectively. This sensory input to the medullary integrator represents the most important component in regulating respiration on a breath-to-breath basis. The peripheral receptors are more proficient in responding to abrupt changes in the PCO2, whereas the central receptors respond to changes in PCO2 over longer periods. If CO2 is voluntarily inhaled, ventilation will increase in proportion to the increase in the fractional composition of CO2 in the inspired gas mixture If neural afferents from the peripheral receptors are cut, the ventilatory response to CO2 is only slightly diminished (10% to 20%). the central chemoreceptors account for a sizable portion of the ventilatory response to CO2. The increased ventilation that accompanies an elevation in arterial H+ concentration or a decline in PO2 are largely mediated via the peripheral receptors. The hydrogen ion does not readily traverse the BBB and the central chemoreceptors are incapable of detecting changes in oxygen tension. 11. Lung and Thorax - the H & P
1. List the subdivisions of the parietal pleura and specify their locations in the pulmonary cavity; specify the locations of the costodiaphragmatic and costomediastinal recesses.
The parietal pleura divides based upon the part of the thoracic cage that it's against. Green at the bottom is the diaphragmatic pleura. Anything that's against the ribs, is the costal pleura. blue the solid pinkish orange line is the mediastinal pleura. The red dotted line is called the endothoracic fascia. the glue that holds the pleura against the body wall. without that the pleura doesn't really stay adhered to the wall as effectively. the top yellow region has no rigid body wall like the diaphragm, the rib cage or the mediastinum for it to be adhered to is the cupula or the suprapleural membrane. the fascia that's anchoring it is Sibson's fascia that is thick.
13.Rationalize the mechanism by which i) allergy immunotherapy and ii) the hygiene hypothesis provide protection against allergens. Allergy immunotherapy (Allergy shots):
The patient is administered small amounts of allergen, increasing in dosage over an extended period of time (or using the same dosage but decreasing the length of time between shots) in an attempt to desensitize the patient to the allergen.
Diaphragm
The principal muscle of inspiration Separates thoracic from abdominal cavity. Converts thorax into closed chamber Downward movement of diaphragms causes volume of thoracic cavity of lungs to increase. ⅔ of tidal volume Motor innervation from C3-5 → Phrenic nerve
Identify and describe the actions of the different respiratory muscles responsible for lung inflation and deflation
The respiratory muscles lack inherent rhythmicity. They depend on motor nerve impulses to initiate contraction and relaxation. The nerve impulses initiating contraction of the respiratory muscles originate in the medullary region of the brain stem.
Unique aspects of prokaryotic metabolism
The way a bacteria uses nutrients/enzymes can serve as key diagnostic tests (ex. differential media) Enzymes/Processes that are unique to the bacteria can be targets for antibiotics (ex. 70s ribosome for translation, enzymes for LPS or Peptidoglycan synthesis)
Type II Hypersensitivities:
These immune responses occur when IgM or IgG antibodies bind antigens on cells, tissues, or the extracellular matrix (ECM). This results in tissue damage through complement activation, inflammation, or phagocytosis but they can also be autoreactive and promote or inhibit host cell function as in Myasthenia Gravis or Graves disease.
Acute Sinusitis
Thickening of sinus mucosa (non-specific finding) Air fluid level is indicative = specific for acute
9) Draw the oxyhemoglobin dissociation curve and state the physiological significance of the sigmoidal shape.
This curve shows the amount of O2 unloaded at a given O2 pressure. The sigmoidal shape has 2 significance:
Be able to recall clinically relevant respiratory anatomy
Thorax Sternum Manubrium Sternal angle Body of sternum Xiphoid process Ribs 1-7 8-10 11, 12 Dorsal vertebrae Scapulae
List the physical and physiological factors that can alter airway resistance, Physical factors
Thus, radial traction dilates airways during inspiration to reduce airway resistance; the reverse occurs during expiration. In addition, the small membranous airways are readily distensible and collapsible, so their diameter is greatly influenced by transmural pressure. Recall that as the lung inflates, intrapleural pressure becomes increasingly subatmospheric, so transmural pressure increases to enlarge the airway lumen. In contrast, during expiration, especially a forced expiration, transmural pressure decreases, so airways are narrowed and the resistance to airflow increases. Thus, both radial traction and transmural pressure increase during lung inflation, increasing airway diameter and reducing frictional resistance to airflow. The opposite occurs during expiration.
7. Rationalize the roles each of the four cardinal signs of inflammation play in the immune (inflammatory) response and how the various cells and cell products which contribute (mast cells, macrophages, neutrophils, eosinophils, granule components, cytokines).
To clear extracellular pathogens an inflammatory response is essentially an increase in leukocytes within tissues (infected or non-infected), and increase in fluid in the tissues (edema). There are 4 cardinal signs of inflammation: redness (rumor), swelling (tumor), heat (calor), and pain (dolor); While neutrophils and macrophages are the primary immune cells involved in the inflammatory response, other immune cells play key roles in this process.
Discuss Ohm's law and Poiseuille's relationship as methods to measure lung airway resistance, Ohms Law
To compute total airway resistance in man, the pressure difference between the mouth and alveoli should be measured at a given flow. While it is difficult to measure alveolar pressure directly, a subject can be placed in a whole body plethysmograph. The plethysmograph allows alveolar pressure to be measured indirectly, so airway resistance can be estimated using Ohm's equation.
List two factors that contribute to frictional resistance associated with lung ventilation,
Total pulmonary frictional resistance 20% tissue resistance = little significant Outer surface of the lungs side over the inner chest wall even though there is intrapleural fluid that prevents most of this. It only accounts for a small amount. Abdominal cavity - as the diaphragm descends during inspiration it compresses the abdominal contents. Thus frictional resistance is encountered as abdominal organs are displaced and mover over one another. 80% airway resistance = most significant Amount of frictional resistance as air moves b/w the mouth and alveoli depends on the linear velocity of airflow. Can be increased by pulmonary disorders such as asthma that narrows the airways. 2 ways to determine this: Ohms law and Poiseuille's Law
Mucociliary transport mechanisms
Tracheobronchial secretions Cilia Defects Cilia toxic Viruses, mycoplasma pneumonia Intrinsic cilia defects Chronic inflammation (smoking) Kartagener syndrome Potential infection problem Stagnant secretions Bronchitis, bronchiectasis, sinusitis Cystic fibrosis - Cilia toxic factor secretions - Tenacious secretions - Infection (mucoid form pseudomonas)
Base substitutions
Transitions: purine to purine, or pyrimidine to pyrimidine Transversions: purine to pyrimidine (or vice versa) Silent, missense, nonsense mutations (informational changes) Gene products not significantly affected
PARENCHYMAL DISEASE
Tuberculosis Lung abscess Pneumonia Mycetoma ("fungus ball") Miscellaneous Goodpasture syndrome Idiopathic pulmonary hemosiderosis Granulomatosis with polyangiitis (Wegener granulomatosis)
Percussion:
Tympany Resonance Hyperresonance Dullness Flatness
Acid fast stain
Used for mycobacterium Carbolfuchsin -- red = acid fast bacteria
Nuclear medicine ventilation/perfusion scan
Used to assess for pulmonary embolism Replaced with CTA (CT Angiography) but now making a comeback because of less radiation. Especially used when - antecubital IV site can not be obtained, patient has allergy to iodinated contrast. Perfusion Scan‐ evaluates lung perfusion through the deposition of microaggregates of albumin labeled isotope (MAA). This is reflective of blood flow to the lungs. Ventilation scan: Inhales Xenon 133 or technetium‐99 aerosol
Community-acquired acute/subacute pneumonias ('atypical')
Usually non-abrupt clinical course (less productive sputum, SOB, etc.) and higher likelihood of generalized symptoms (headache, sweating, myalgias, etc.) Often viral in etiology (influenza A/B, respiratory syncytial virus, rhinovirus, adenovirus, human metapneumovirus, etc.) or 'unusual,' less virulent bacteria (Mycoplasma, Chlamydia) Causative organisms may be more difficult to identify in a laboratory setting Range from self-limited and mild (many upper and lower viral infections) to severe epidemics (influenza) Grossly affected lungs will appear red and congested → as evolves foci of bronchopneumonia
Aspiration pneumonias
Usually seen in pts w/ debilitation, dementia, unconsciousness (stroke), or in those w/ repeated vomiting (alcohol abuse), or underlying cough or gag reflex impairment These pneumonias are typically necrotizing and abscess-forming Aspiration pneumonia is a common cause of disease that pushes a patient (possibly with underlying disease) into organ failure, which then taxes other organ systems leading to multisystem organ failure and death. Causes are anaerobic oral flora (see above in Necrotizing category) or 'colonizing' aerobes: H. influenza, S. pneumonaie, P. aeruginosa, S. aureus
Alveolar or physiological shunt
V/Q mismatching - combination of areas in the lung with low and high V/Q. Normal V/Q→ low O2 capillary blood w/ PO2 of 40 is exposed to alveolar PO2 of 100. Gas exchange occurs and blood has an O2 content of around 19.5% and PaO2 of 100, meaning it's appropriately ventilated and perfused. Low V/Q → capillary blood flow is normal but ventilation is impaired due to obstructed airway. After gas exchange there is lower than normal PaO2 of 50 and 16% O2 content in capillary. V/Q ratio is 0.1 or 1/10. High V/Q → normal ventilation, blood flow is obstructed. V/Q is 10 and a greater than normal PO2 of 130 torr and content of 20%. However the pulmonary vein blood perfusing alveoli of different V/A mixes to yield PO2 of 64 and content of 17.9%.
7. Describe the regional differences in alveolar ventilation and explain the basis for these differences.
Ventilation increases the lower we are in the lung. This is due to GRAVITY!! Also the base of the lung has smaller alveoli—>more surfactant—> Lower pressure and more compliant—> fill 1st.
Eval: Fever patterns
Viral infections: fever tends to decline over a week. Bacterial infection: fever resolves after initiation of antimicrobial therapy. Intermittent fever: period of normal temperatures within a day; wide fluctuations termed septic or hectic fever. Sustained fever: persistent and does not vary by more than 0.5°C/day. Remittent fever: persistent and varies by more than 0.5°C/day. Relapsing fever: febrile periods that are separated by intervals (days/weeks) of normal temperature. Biphasic fever: single illness with 2 distinct periods. Periodic fever: fever syndromes with regular periodicity.
PE: fever
Vitals!!! T/P/R/B Don't Forget Weight. General: How does the Baby/child appear? Any signs of sepsis as described above? HEENT: Fontanelle TM's Mouth for lesions, dryness, thrush,etc. Nasal Congestion HEART: Rate/Rhythm/Murmurs/Pulses Lungs: Breath Sounds/ Wheezes/ Crackles/ Transmitted Upper Airway Sounds Abdomen: Palpation/Auscultation EXT: Check perfusion/ Movement/Erythema or edema Genitalia: Male vs Female/testes down or up. Skin: Rashes/Mottling/Cyanosis/Erythema NEURO: Tone/ grasp/ suck Reflexes
How to distinguish between minor and massive
Volume is difficult to quantitate therefore: Magnitude of effect is important Hemodynamics Gas exchange Aspiration of clots Need for transfusion
Total ventilation (minute ventilation)—>
Volume of AIR (OLD + FRESH or Tidal volume) in the lungs/minute. Ve= TV x f . Va: Alveolar ventilation / Vd: Dead space volume / Ve: Minute ventilation / f: Breath frequecy
3. Distinguish between total ventilation, alveolar ventilation, and dead space ventilation. Alveolar Ventilation—>
Volume of FRESH air introduced into the gas exchanging regions of the lungs/minute. Va= (TV-Vd) x f
Dead space ventilation—>
Volume of OLD air in the dead space/minute. Vd= Vd x f
Tidal volume (TV)—>
Volume of air in and out of the lung OR volume passing through the mouth/nose with each normal breathing.
4. Understand the relationships between anatomic dead space, tidal volume, respiratory rate and alveolar and total ventilation. Tidal volume (TV)—>
Volume of air in and out of the lung with each NORMAL breath. (around 450mL) For relationship look at question ABOVE.
Residual volume (RV)—>
Volume of air in lung at the end of max expiration.
FRC—>
Volume of air in the lung after a normal TV expiration. All elastic forces are balanced. FRC= ERV+RV
Total lung Capacity (TLC)—>
Volume of air in the lung after maximum inspiration. TLC=IRV+TV+ERV+RV.
Classification of hypoxemia
Without hypercapnia: PaO2 is low, PaCO2 is low or normal Due to V/Q mismatch, diffusion defect, shunt With hypercapnia: Due to hypoventilation like COPD
Bruton's agammaglobulinemia:
X-linked disorder which results from a mutation in a tyrosine kinase specific to B cells (Bruton's tyrosine kinase, Btk). Without this enzyme, there is a loss of the proliferation and differentiation signals provided to the developing B cells resulting in a B cell block at the checkpoint between pre-B cells and immature B cells. Thus, there is a decrease in the number of mature B cells in circulation and a defect in the humoral immune response. Males are primarily affected and develop multiple, recurrent bacterial infections of the respiratory tract and skin starting a few months after birth. Individuals with this immunodeficiency are more susceptible to recurrent bacterial and viral infections such as otitis media, pneumonia, and pharyngitis. Treatment involves prophylactic antibiotics and IVIG (intravenous immunoglobulin) infusions. Death in childhood occurs from respiratory failure due to complications of repeated lung infections.
Fetal breathing starts
at 14 wks gestation and stops during labor Surfactant produced around 20 wks
Transient tachypnea (TTN) PP:
delayed clearance of fetal alv fluid Perfusion of poorly ventilated alveoli leads to hypoxemia Accumulation of fluid in the peribronchiolar lymphatics causes air trapping
Mass—>
abscess, hematoma, thyroid, tumor (SCC, lymphoma) Foreign body Paralyzed vocal cords.
Mycobacterium TB:
acid-fast smear, culture are definitive dx, tx w/ RIPE Reactivation in apex, initial inf in lower lobes AIDS might have miliary TB
8. Compare the cells of the adaptive immune system in respect to their: i) antigen receptors, ii) products, and iii) functions. Contrast how the antigen receptors on adaptive immune cells are different from those on the innate immune cells.
adaptive immune response takes longer to produce than the innate immune response because the innate cells (ie. a dendritic cell or a macrophage) must first capture the antigen, travel through the body using the blood or lymph, and enter the secondary lymphatic organs where they can "show", or present, the antigen to a T cell The T cell specific receptor is the T cell receptor (TCR B cell specific receptor is the antibody (Ab, or immunoglobulin, Ig). Both of these receptors are very specific in the molecules that they recognize. And both can recognize the host preventing autoimmunity usually. T cells have two classes helper T cells (Th) CD4 and cytotoxic T cells (CTLs). CD8 To stimulate the effector functions of these T cells, the antigen must present the peptide in either an MHC I or MHC II molecules. Recall, each of these molecules is produced by the transcription and translation of HLA genes, an important consideration in transplants. Additionally, these MHC molecules are used to present intracellular and extracellular peptides, respectively.
Understand the relationship transpulmonary pressure, alveolar pressure, intrapleural pressure, and lung volume during a normal tidal inspiration and expiration.
air flows into lung when P outside (atm) is BIGGER than P inside (alv), get bulk flow** Inspiration: diaphragm goes down, chest out, volume up, pressure decrease Expiration: diaphragm goes up, chest in, volume down, pressure increase Point 1 of figure At the end of a normal expiration (just before inspiration), airways open and no air flowing, then Patm= Palv. Intrapleural pressure is just slightly below atmospheric pressure. If Patm and Palv are equal then distending pressure= Pinside-Poutside= lung distending pressure= transpulmonary pressure(PTP) Air flows into the lungs during inspiration bc of C above, Palv decrease due to inc in lung volume Point 2 of figure At the end of a normal inspiration Patm and Palv are again equal but now intrapleural pressure is more negative relative to atmospheric pressure and distending pressure is much larger. Air flows out of the lungs during expiration bc of D above, volume dec in alv & palv inc
2. Distinguish between anatomic and physiologic dead space. Anatomic dead space—>
all the air in the conducting system (nose—>terminal bronchioles). NO GAS EXCHANGE here!!!
Periodic breathing:
alternating breaths, pauses in breathing (5-10 seconds) Normal, does not require tx unless very severe desaturation w/ lung disease More common in premature, resolves by 3 mos
Alveolar dead space—>
amount of air that does not participate in gas exchange (it can be due to either capillary or alveolar obstruction or a disease that prevents gas exchange)
Clostridium—>
anaerobic spore forming rod
3) Specify the surface locations of auscultation of the following structures:
apex of right lung, apex of left lung—> R/L Supraclavicular superior lobe of right lung—> Rib 1-4 superior lobe of left lung—> Rib 1-6 middle lobe of right lung—> Rib 4-6 inferior lobe of right lung, inferior lobe of left lung —> rib 6-10
Explain what it means to say that the normal barometric pressure at sea level is 760 mmHg.
at sea level, the average total pressure exerted by the gases comprising the earth's atmosphere was sufficient to elevate a column of mercury (Hg) 760 mm of Hg or Torr. 760 Torr is equal to 1 Atmosphere (ATM) and to 101.3 kilo Pascals (kPa).
5. Discuss the components of the immune system and mechanisms available to the host for eliminating extracellular and intracellular pathogens. Extracellular pathogens (bacteria)
can be captured and phagocytosed by macrophages, dendritic cells, neutrophils, or eosinophils, or can cause activation of mast cells
Intracellular pathogens (viruses)
can be eliminated by natural killer (NK) cells which destroy the virally infected host cell or, cytokines which make the host cell environment unfavorable for pathogen reproduction, thereby inducing an antiviral state. Or can also be destroyed by cytotoxic T cells (CTLs) of the adaptive immune system.
Strep—>
chained cocci, Cat-, strictly fermentative
Pasteurellaceae—>
coccobacilli and pleomorphic (diff size and shape) // P.multocida, H.influenzae, H.ducreyi
Breathing stim by
cooling, PG and adenosine decrease Air fills lungs → lower pulm vascular R → more blood flow Placental circulation removed → lower systemic vascular R
Causes of hypoxemia:
decrease is PiO2 (high altitude), V/Q mismatch, R → L shunt Alv hypoventilation (high PAO2) (LOW) Severe lung disease, CNS depression, thoracic trauma, structural Decrease in diffusion: thickened membrane, decreased surface area or time (tachyarrhythmia), slow RBC O2 binding
8. Describe the effects of injury to one or both phrenic nerves as it relates to function of the diaphragm
diaphragm is innervated by the phrenic nerve which comes from C3-5 nerve Roots When damaged pain is felt in the neck and upper shoulder Normally resting respiration indicated by the purple lines in both diagrams and in inspiration are the red lines. the diaphragm moves inferiorly during inspiration and it moves relatively uniformly on both sides when the diaphragm contracts normally. If there is paralysis of the diaphragm on one side, you will still to some extent get flattening of the diaphragm, but it wont be uniform
5 times rule:
estimate PaO2 for a pt on supplemental O2 by multiplying O2% by 5 Ex: 60% O2 would have PaO2 about 300 mmHg bc 60*5=300
Clinical/Diagnosis
fever , purulent sputum, decline in O2, tachypnea (higher the RR the more severe illness) X-ray - new infiltrate Lab - leukocytosis, or leukopenia w/ left shift (more bands -- worse prognosis) Microbiology - endotracheal aspiration Bronchoalveolar lavage (BAL) Extra (don't need to memorize below - but know the chart above) Lecture 10 (session 2): Sepsis
2. Macrophages
found throughout connective tissue, organs, as well as lymphoid tissue. four major functions: 1) phagocytosis and subsequent production of the respiratory burst to eliminate the ingested pathogen, 2) production and secretion of cytokines and chemokines to activate immune cells (NK cells, B cells, and T cells) or promote inflammation, 3) present antigens to T cells, and 4) manage wound repair by stimulating angiogenesis and fibrosis.
PRRS
host cells such as phagocytic cells, epithelial cells, hepatocytes, and leukocytes have PAMP receptors called PRRs examples:TLR, lectin, and NOD-like receptor, and are located in the plasma membrane, cytosol, AND endosomal membrane (good because some PAMPS aren't available until after destruction of pathogen) Results of PRR-PAMP interaction: the production of cytokines (promoting inflammation, inducing an antiviral state), and an increase in cell adhesion molecules and other molecules required for an adaptive immune response. Help w/ intra and extracellular infxns Intracellular infxns are controlled w/ secretion of antiviral proteins: type 1 interferons Ifn-a from epithelial cells, b cells, dendritic cells and macrophages Ifn-b from fibroblasts Host cells can respond to these by producing enzymes that inhibit protein synthesis and degrade viral mRNA inducing an antiviral state. These virally infected cells can therefore be eliminated by NK cells or phagocytosed and destroyed by a dendritic cell or a macrophage.
Congenital lobar overinflation (Emphysema):
hyperinflation of 1+ lobes due to obstruction of airway Compresses other lobes, asymptomatic at first but progressive Symptomatic requires resection
7. Describe how the appearance of the costophrenic angle might change on an upright x- ray due to fluid accumulation in the recess.
if you send somebody for an x-ray and they've got fluid in that costodiaphragmatic recess there will be blunting of that costophrenic angle.
X ray/CT Imaging:
images show what the CT will show at the indicated X-ray level Lecture 18 week 2: The airways
The Hering-Breuer Inflation reflex (also called inhibito-inspiratory reflex)
initiated by stretch receptors in the smooth muscles surrounding both large and small airways. With lung inflation, these stretch receptors are stimulated and send neural signals via vagal afferents are inhibitory to the pontine apneustic center. They terminate of inspiration
Hering-Breuer Deflation reflex (or excito-inspiratory reflex).
initiated either by decreased activity in the airway stretch receptors involved in the inflation reflex or by stimulation of other proprioceptors that are activated by lung deflation. This information is conveyed via vagal afferents to the brain stem respiratory centers to encourage inspiration.
4. Eosinophils
innate immune cells involved in allergies and asthma and destruction of helminths and parasites. have preformed granules in their cytoplasm Eosinophils are activated in a similar manner to mast cells: need to be sensitized by IgE binding to Fc receptors on eosinophils during a primary antigen exposure. Upon re-exposure to the same antigen, the antigen binds to multiple IgE antibodies, cross-linking the Fc receptors on the surface of the eosinophil causing it to degranulate express an IL-5 receptor, which must be engaged before the granules can be released.
10.Explain the process and purpose of: i) isotype switching, and ii) transcytosis including the important molecules or enzymes, cells, cytokines, and antibody isotype produced (or involved) in your discussion. Isotype switching
involves T-dependent B cells (usually follicular B cells), helper T cells, and the cellular enzyme AID (activation induced deaminase) which functions to recombine the constant regions of the heavy chain genes.
Alv-arterial gradient
is diff between PaO2 and PAO2 PAO2 = PiO2 - (PaCO2 * 1.25) bc 1.25 is inverse of 0.8 (normal R) Normal is (age/4) + 4
FiO2
is fraction of O2 (0.21 at sea level), PaO2 (alveolar) increases w/ FiO2
Acute resp failure
is if PaO2 <50 mmHg or PaCO2 >50 mmHg
Define hypo- and hyperventilation and explain how they affect alveolar partial pressure of oxygen (PAO2) and carbon dioxide (PACO2). Hyperventilation
is when alveolar ventilation exceeds metabolic rate or exceeds the demand for either oxygen uptake or carbon dioxide removal. ↑ PAO2 that approaches but never reaches the PIO2 as VA increases. ↓alveolar PCO2 declines with hyperventilation so that doubling alveolar ventilation from the resting rate reduces the PACO2 by about one half.
Chronic granulomatous disease:
mutation in the phagocyte oxidase enzyme of phagocytic cells (autosomal recessive or X-linked), thus difficulty stimulating the respiratory burst and therefore the production of reactive oxygen species necessary to destroy the invading pathogen. More immune cells (macrophages and T cells) are recruited in an attempt to eliminate the pathogen, eventually forming a granuloma as a result of the positive feedback loop formed between these two cells. As such, these individuals often present with recurrent infections with catalase positive bacteria and fungi. Treatment is with prophylactic antibiotics and antivirals, IFN-γ, or a bone marrow transplant.
Epiglottitis—>
normal epiglottis looks like pinky (anterior cervical tissues C2<7mm and C5-C6<21mm) but abnormal one looks like thumb.
Respiratory distress syndrome: PP:
not enough surfactant → atelectasis, inflammation Surfactant reduces surface tension of alveoli, prevents collapse Made by type II alveolar cells around week 20 of gestation Inadequate surfactant activity results in high surface tension Causes atelectasis, low lung volumes, and decreased compliance Can't clear fluid as well, get edema → hypoxemia/hypoventilation CP: Premature baby w/ resp distress at birth, decreased breath sounds Tachypnea, nasal flaring, grunting, retractions, cyanosis Gets worse for first couple days CXR: small lung volume, ground glass appearance
Normal ABG:
pH = 7.35-7.45 PaO2 = 80-100 mmHg 70 normal for elderly 65+ Hypoxemic drive activates when PaO2 50-60 mmHg 40 mmHg see cyanosis, 30-35 bad for heart/brain, 20 is dead PaCO2 = 35-45 mmHg Bicarb calculated 22-26 mEq
LARGE AIRWAYS DISEASE:
pharynx, larynx and trachea Usually use X-ray 1st followed by CT Vocal cord paralysis—> assess the recurrent laryngeal nerve (RLN-branch of the Vagus nerve) with CHEST CT. Right RLN passes under the right subclavian artery Left RLN passes under the aortic arch
Define and distinguish three types of right-to-left heart shunts. Right-to- left shunts,
poorly oxygenated blood is added to oxygenated blood just before the left heart pumps it to the tissues of the body. Three types of right-to-left shunts are generally recognized that account for the alveolar to systemic arterial PO2 difference (A - a PO2 difference).
4. Define pleural cavity, pulmonary cavity, and thoracic cavity; be able to use these terms
properly when discussing the anatomy of the thorax. The pleural cavity is between the parietal and visceral layers of pleura. Thoracic cavity, also called chest cavity, the second largest hollow space of the body. It is enclosed by the ribs, the vertebral column, and the sternum, or breastbone, and is separated from the abdominal cavity (the body's largest hollow space) by a muscular and membranous partition, the diaphragm. The right and left pulmonary cavities, which flank the mediastinum laterally and anteriorly, extend superiorly above the costal cartilages of the first rib and inferiorly to the thoracic diaphragm . Each pulmonary cavity contains a lung and bronchial tree and a pleural sac.
Pneumocystis jiroveci (PCP):
protozoa, exposure in childhood, latent → reactivation Most common opportunistic pathogen in AIDS pt, see bilateral interstitial infiltrate Usually in cell-mediated deficient pts Hypoxia as inf goes on, get sputum for dx
CMV
rarely causes pulm inf in AIDS pt, mostly in neutropenic pts See retinitis and colitis in AIDS pts
Outcomes/complications of acute pneumonia
resolution= any exudate is degraded and lung architecture restored Organization: inflammatory process→ grey hepatization → fibrosis Pleural involvement: pleuritis (inflammation of pleura) or empyema (a gross of collection of pleural space-located pus) are possible; may lead to scarring Necrotization: intrapulmonary abscess formation and/or cavitation
12. Explain the hypersensitivity reactions affecting the respiratory system discussed in this lecture (Type I, Type II, and Type IV; asthma, allergies, anaphylaxis, urticaria, Goodpasture syndrome, and mycobacterium tuberculosis) including their: i) classification, ii) pathogenesis, iii) symptoms, iv) diagnosis, and iv) potential treatments. Type I Hypersensitivities:
result from the activation of sensitized mast cells or eosinophils and involve the antibody isotype IgE.
3. Describe and localize the brain stem integrating centers responsible for producing the spontaneous rhythmicity of breathing.
sensors send signals via vagal afferent nerves to influence breathing rate and depth. these vagal afferents innervate the brain below midbrain level. the lower two-thirds of the pons encourages inspiration because without input from vagal afferents or the upper pons, apneusis was observed. Thus, the lower two-thirds of the pons is designated as the Apneustic Center, while the upper one-third is called the Pneumotaxic Center. The transection studies suggest that both the pneumotaxic center and vagal afferent nerves innervate the apneustic center to diminish inspiratory drive. apneustic center appears to continuously promote inspiration and requires periodic inhibition from the pneumotaxic center and vagal afferents for expiration to occur. so the pneumotaxic center and vagal afferents collectively constitute a "cut-off" switch for the apneustic center. When inspiration is terminated, expiration can occur. vagal afferents likely innervate the pons as opposed to the medullary region. However, a transection across the lower border of the medulla (transection #5) results in apnea. the minimal neuronal pools necessary for spontaneous breathing reside in the medullary portion of the brain stem (Medullary Center) Although neuronal pools of the medullary center alone appear sufficient to initiate and maintain sequences of inspiration and expiration, input from the pontine pneumotaxic and apneustic centers are essential for rhythmic and coordinated breathing.
Chest CT hemoptysis
superior in detecting and excluding malignancy vs. fiberoptic bronchoscopy (FOB) however, FOB is useful in finding small endobronchial lesions and in establishing a definitive tissue diagnosis Bronchoscopy: Can be diagnostic and therapeutic Malignancy is one of the most common causes of hemoptysis, and bronchogenic carcinoma accounts for most of the cases. Extrathoracic malignancies especially melanoma and breast, colon, renal may also cause hemoptysis because of their propensity to metastasize to endobronchial locations.
Eosinophils can also produce
the same lipid mediators and cytokines as mast cells can phagocytose and release antihistamines (arylsulfatase) to control inflammation, and extravasate out of blood vessels, enter inflamed tissues, and phagocytose antigen-antibody complexes.
3. Define a bronchopulmonary segment.
the smallest functional unit of the lung you can surgically remove one and separate it from the other side without negatively impacting the function of neighboring segments because it has its own bronchus, its owner arterial supply, its own lymphatic drainage and its own nerves each lung is comprised of 10 bronchopulmonary segments left lung has two lobes and each lobe has five segments. right lung has three lobes: the upper lobe has 3, the middle lobe has two and they lower lobe has five
ESOPHAGUS—>
transients from mouth and URT
Understand how deficiencies in cell-mediated immunity can lead to certain infections
usually genetic: mostly inf w/ intracellular orgs Digeorge syndrome, Wiskott Aldrich, Ataxia telangiectasia, AIDS → life threatening resp and generalized infxs w/ obligate intracellular orgs GNB, listeria, cryptococcus, Histo, Pneumocystis, Toxoplasmosis, strongyloides, S. Pnuemoniae, S. aureus, H. influenzae,mycobacteria, CMV, candidasis, cryptosporidium
3. List the 4 major causes of hypoxemia Diffusion Impairment
↓PaO2 and a normal PAO2 Normal or ↓PaCO2 ↑P(A-a)O2 gradient Rarely the sole cause of hypoxemia
3. List the 4 major causes of hypoxemia Hypoventilation
↑PACO2 and PaCO2 ↓PAO2 and PaO2 Normal A-a gradient when occurs acutely PAO2 and PaO2 (but not the hypoventilation) can be corrected by ↑FIO2.
SPORE-FORMING GRAM+ RODS: Bacillus
—> aerobic // B.anthrax—> zoonotic anthrax // B.cereus—> enterotoxin-mediated food poisoning
3. List the 4 major causes of hypoxemia Shunt
↓PaO2 ↑P(A-a)O2 gradient Responds poorly to increases in FIO2 Not corrected by 100% O2
3. List the 4 major causes of hypoxemia Low V/Q mismatch
↓PaO2 due to ↓V/Q alveoli ↑PaCO2 ↑P(A-a)O2 gradient Responds well to small increases in FIO2 Completely corrected w/ 100% O2