Week 9 Flashcards
1
Q
List the anatomic/physical factors that make up the respiratory tract defense mechanisms.
List three of them and how they work.
A
- Physical and anatomic barriers
- Branching of airways – filters the air
-
Cough reflex – removes filtered particles
- Afferent irritant receptors stimulate efferent vagus response, leading to contraction of diaphragm and cough
- Mucociliary transport – moves particles trapped on mucus layer up and out
2
Q
List some innate cell types.
A
Antimicrobial peptides, NK cells, phagocytic cells (macrophages, PMNs), dendritic cells
3
Q
Where are antimicrobial peptides located in the respiratory system? Name 4 of them and each of their functions.
A
- Antimicrobial peptides – in the sol layer of the mucus (layer closest to cell membrane)
- Lysozyme – in proximal airway and lyses bacteria
- Lactoferrin – promotes neutrophil superoxide response
- Defensins – secreted peptide that increases cell wall permeability in foreign cells
- Collectins – surfactant protein that aggregates microbes
4
Q
What are NK cells?
A
NK Cells – kill virus infected cells
- Resident cells
5
Q
What do macrophages do in the respiratory system?
A
- Macrophages
- Prevents infections
- Homeostasis – “inhibit” immune responses
- Can process 109 bacteria without eliciting further immune response
- Keeps lungs sterile and not inflamed
6
Q
What do PMNs do in the respiratory system?
A
- Responds to established bacterial infections
- In normal state, few are present in small airways and alveoli
- In infection, activated macrophages recruit PMNs to alveolar spaces
7
Q
What do dendritic cells do in the respiratory system?
A
- Dendritic cells – process and present antigen to adaptive immune cells
- Present in alveolar walls
- Sample environment and present antigen to T lymphocytes
8
Q
In the alveolar space, where are the following located:
- type I pneumocyte
- type II pneumocyte
- alveolar macrophage
A
9
Q
What are the two types of systems involved in the adaptive immunity? What cells are involved in each?
A
Adaptive
- Humoral Immunity
- B cells
- ABs
- Cellular immunity
- T-cells
10
Q
What is the funcitonal of humoral immunity and what cells are a part of it? What do they each do and where are they located?
A
- Humoral immunity – prevent microbe entry, clear extracellular bacteria, +/- fungi
- B cells
- ABs – agglutinates microorganisms, neutralizes
- IgA – in nasopharynx/upper airways, protects mucosal surfaces
- IgG – lower airways, complement activation
11
Q
What is the function of cellular immunity? What cells are a part of this system?
A
- Cellular immunity – intracellular bacteria, viruses, fungi (with phagocyte help)
- T cells – helper, cytotoxic, regulatory
12
Q
What are the two methods of physical clearance? What infections can occur if these mechanisms fail?
A
Physical Clearance
- Impaired cough = aspiration pneumonia
- Impaired mucociliary clearance = bacterial infections
13
Q
Provide 4 clinical examples for impaired cough and what infection occurs?
A
-
Impaired cough = aspiration pneumonia (anaerobes)
- Clinical examples
- Muscular dystrophy (impaired diaphragm), tracheostomy, quadriplegia, vocal cord paralysis
- Clinical examples
14
Q
Provide a genetic and an evnironemental clinical example for impaired mucociliary clearance. What type of infection generally occurs with impaired mucociliary clearance?
Name some clinical consequences of impared mucociliary clearance. A specific syndrome?
A
-
Impaired Mucociliary clearance = bacterial infections
- Clinical examples
- Genetic: primary ciliary dyskinesia (PCD)
- Environmental: viral infection, smoking, general anesthesia
- Clinical consequences
- Kartagener’s syndrome: PCD with situs inversus (internal organs are flipped) – rare
- Recurrent infections
- Clinical examples
15
Q
What infections are common in phagocytic defects? What cells are affected in phagocytic defects (2)?
A
-
Phagocytic defects = fungal, bacterial infection
- Clinical examples
- Macrophage deficiency
- Neutrophil deficiency
- Clinical examples
16
Q
What can cause macophage deficiency? What type of defect is macrophage deficiency?
A
-
Phagocytic defects = fungal, bacterial infection
- Clinical examples
- Macrophage deficiency
- Impaired killing – viral infections, smoking, hypoxia, starvation, alcoholism
- Impaired migration/function – chronic systemic steroids
- Macrophage deficiency
- Clinical examples
17
Q
What can cause neutrophil deficiency? What type of defect is neutrophil deficiency?
A
-
Phagocytic defects = fungal, bacterial infection
- Clinical examples
- Neutrophil deficiency
- Decreased numbers: leukemia, chemotherapy, congenital
- Impaired migration/function: congenital
- Neutrophil deficiency
- Clinical examples
18
Q
What are the clinical consequences of phagocytic defects?
A
- Clinical consequences: bacterial bronchitis/pneumonia (macrophages deficiency) and bacterial infections/fungal infections (neutrophil deficiency)
19
Q
What type of infections are common with NK cell defects?
A
Viral infections
20
Q
What kind of infections do you get with humoral cell defects?
A
- Humoral defects = bacterial (especially encapsulated) infections
21
Q
What are some examples of humoral defects? Name one congenital and two secondary.
A
-
Humoral defects = bacterial (especially encapsulated) infections
- Clinical examples:
- Congenital: hyper-IgM syndrome
- Secondary: nephrotic syndrome (kidney damage), chemotherapy
- Clinical examples:
22
Q
What infections occur as a consequence of humoral defects?
A
-
Humoral defects = bacterial (especially encapsulated) infections
- Clinical consequences
- Recurrent bacterial respiratory infections
- Bronchiectasis
- Clinical consequences
23
Q
What are combined defects?
A
- Combined defects = features of both humoral and cellular immunity
24
Q
What are antimicrobial peptide defects (4)? Name a clinical example and some clinical consequences?
A
- Antimicrobial peptide defects (defensins, lactoferrins, collectins, lysozymes)
- Clinical examples
- Cystic fibrosis
- Clinical consequences
- Require defect in multiple peptides for a true immunodeficiency
- Defensin defects: severe respiratory infections
- Clinical examples
25
Name 5 anti-histamines.
MNEMONIC ALERT (may or may not help): "**_C**_an't _**D**_o _**H**_istamines _**F**_or _**L_**ife"
* **_C_**etirizine
* **_D_**iphenhydramine
* **_H_**ydroxyzine
* **_F_**exofenadine
* **_L_**oratadine
26
What is the general mechanism of action of antihistamines?
Competitive H1 receptor (Gq receptor); although increase in intracellular Ca2+, histamine stimulation causes production of prostacyclin and NO, outweighing histamine’s vasoconstrictive effects
27
What are the uses of antihistamines?
What are the adverse effects of antihistamines?
Use: Allergy-mediated pathologies
Adverse Effects: Diphenhydramine and hydroxyzine have anticholinergic effects (aka sedating)
28
Name 2 decongestants
* Pseudoephedrine
* Phenylephrine
29
For decongestants (pseudophedrine, phenylepherine):
* What is the MOA?
* What are the uses?
* What are some adverse effects?
* MOA: Alpha 1 agonists (Gq) – vasoconstriction
* Uses: Used to decrease mucus production
* Adverse effects: Tissue necrosis if use extends past 3 days
30
For intranasal corticosteroid:
* Name one.
* What is the MOA?
* What is its use?
* What are 3 adverse effects?
* Example: fluticasone
* MOA: Transcription factor that decrease capillary permeability, stabilize lysosomes, decrease mucus production
* Uses: Sinusitis
* AE: Candida infection, perforation of nasal septum, bone necrosis
31
For expectorant:
* Name one.
* What is the MOA?
* What is its use?
* Guaifenesin
* MOA: Increase respiratory tract fluid secretions and helps loosen phlegm
* Use: Sinusitis (may help – “expect” it to help)
32
For mucolytic agents:
* Name one.
* What is the MOA?
* What is its use?
* Example: acetylcysteine
* MOA: Splits the disulfide linkages that holds mucus together
* Use: Reduces sputum viscosity to improve secretion clearance
33
For opioid antitussives:
* Name three.
* What are the MOAs?
* What is its use?
* Adverse effects?
* Example: Codeine/Hydrocodone/Dextrmethorphan
* MOA: Acts on Gi receptors to hyperpolarize cell membranes – prevents neurotransmitter release
* Uses: Decreases cough (so people with colds can sleep)
* Adverse effects: Dextromethorphan (seen as DM in cold medications) is very weak; honey more effective
34
For non-opioid antitussives:
* Name one.
* What is the MOA?
* What is its use?
* Adverse effects?
* Example: Benzonatate
* MOA: Topical anesthetic action on respiratory stretch receptors (blocks sodium channels)
* Use: Decreases cough (so people with colds can sleep)
* AE: Sedating
35
# Define the following terms:
* Nasopharyngitis
* Acute rhinosinusitis
* Acute otitis media
* Acute infection pharyngitis
* Rhinitis
* Nasopharyngitis: more commonly known as the Common Cold
* Acute rhinosinusitis: inflammation of the nasal cavity and sinuses
* Acute otitis media: bulging of tympanic membrane (TM) or otorrhea
* Acute infection pharyngitis: inflammation of the pharynx
* Rhinitis: inflammation of nasal cavity
36
What is the epidemiology of nasopharyngitis?
* What age group does it most occur in?
* How does transmission occur and what viruses?
* Epidemiology
* More frequent in children
* Transmission occurs from direct hand-to-mucus membranes (rhinovirus) or small droplet inhalation (only 15 micrometers, does not get into distal airways; influenza, RSV)
37
What is the pathophysiology of nasopharyngitis?
* What does yellow mucus mean? Green mucus?
* What can bradykinin cause?
* Pathophysiology – **VIRAL**
* Virus deposits on nasal/conjunctiva mucosa → attaches/enters to epithelium → virus replicates → epithelial cells release IL-8 and bradykinin → recruitment of PMN
* Yellow mucus = PMN aggregation
* Green mucus = PMN enzymatic activation
* Bradykinin causes dry cough
38
For nasopharyngitis:
* What are the clinical symptoms associated with it?
* Risk factors?
* Complications as a result of the condition?
* Diagnosis?
* Treatment?
* Clinical
* Nasal congestion, sore throat, rhinorrhea, cough, sneezing, +/- headache
* Fever is uncommon but can be present
* Risk factors – exposure to children, parents, stress, lack of sleep
* Complications
* Otitis media, bacterial rhinosinusitis, asthma exacerbation, lower respiratory tract infection (virus affects cilia and can cause severe infection)
* Diagnosis
* Lungs are clear
* Treatment
* Decongestants, analgesics
39
For acute rhinosinusitis, provide pathophysiology of the viral and bacterial types?
* Indicate the 3 microorganisms that cause each
* How long are the symptoms for each? Do they get worse or better?
* What is the method of infection?
* Pathophysiology
* Viral – inoculation via direct mucosal contact
* Rhinovirus, influenza, parainfluenza
* Has \< 10 days of symptoms without worsening
* Bacterial – secondary to viral infection; rare
* *S. Pneumoniae, H. influenza, M. catarrhalis*
* Has ≥ 10 days of symptoms without improvement/double worsening (getting better for a few days and then it gets worse)
40
What are the symptoms associated with acute rhinosinusitis? Differentiate between complicated and uncomplicated bacterial rhinosinusitis. How do you diagnose both?
* Clinical
* Purulent discharge with nasal congestion +/- facial pain, pressure, fullness
* Uncomplicated acute bacterial rhinosinusitis – no evidence that the disease has spread outside of nasal cavity and sinuses
* No culture
* Complicated acute bacterial rhinosinusitis – disease has spread outside nasal cavity and sinuses
* Perform culture
* Possible to get fungal rhinosinusitis
41
What are two complications associated with acute rhinosinusitis? What are the treatments for the conditon (specifically for uncomplicated??)
* Complications
* Osteomyelitis
* Meningitis – sinuses are really close to the brain!
* Treatment
* Decongestants, analgesics
* Antibiotics if bacterial (amoxicillin)
* Uncomplicated may resolve by itself without Abx
42
For otitis media:
* What is the age group that the condition is most common in?
* What are four symptoms?
* How can it be diagnosed? Three indications.
* What are two complications?
* What is the general treatment?
* Epidemiology
* High prevalence in children between ages 6 and 18 months old
* Clinical
* Infants have no way to communicate pain: fever, irritability, headache and ear pain
* Diagnosis
* Bulging of TM and opacity and erythema
* Complications
* TM perforation and hearing loss
* Treatment
* Antibiotics (amoxicillin) or observation
43
Discuss the pathophysiology of acute otitis media. What are the three bacteria involved?
* Pathophysiology
* Bacteria involved: *S. Pneumoniae, H. influenza, M. catarrhalis*
* Occurs often in infants because the Eustachian tube is very horizontal and short (in adults, it is more angled and longer), allowing for easier infections
* URI → travels to Eustachian tube → inflammation/edema → negative ear pressure → bulging of TM
44
For acute infectious pharyngitis:
* What is the age group that the condition occurs in?
* What is the general pathophysiology?
* What microorganisms cause the condition?
* What are two ways to diagnose the condition?
* What is the VERY IMPORTANT COMPLICATION?
* Epidemiology
* School-aged children
* Pathophysiology
* Viral (most cases are viral): part of the common cold
* Bacterial (15% of cases): **Group A Strep, *N. gonorrhoeae***
* Diagnosis
* Throat culture – gold standard
* Rapid antigen test – widely used
* Complications
* **Rheumatic fever (main goal of treatment is to prevent)**
45
For acute infectious pharyngitis, indicate the symptoms associated with bacterial and viral?
* Clinical
* Bacterial
* Age 5-15
* Fever
* White exudate on tonsils
* Tonsillopharyngeal inflammation
* Anterior cervical lymphadenopathy
* Viral
* Conjunctivitis
* Hoarseness
46
Distinguish between allergic rhinitis and non-allergic rhinitis.
Allergic rhinitis:
* Associated pruritus, sneezing
* Have allergic triggers
* Other atopic diseases may be present
* Responds to antihistamines
* Positive allergy testing
* Inflammed turbinate in nose turns bluish/pale color from normal red
* Mast cells release histamine
Non-allergic rhinitis:
* Lack of irritative symptoms
* Mostly irritant triggers
* No other atopic diseases present
* Do not respond to antihistamines
* Negative allergy testing
* Inflammed turbinate without change in color
47
Define basic pleural anatomy
* Anatomy
* Visceral pleura lines the outer layer of the lung
* Parietal pleura line the inner chest wall
* Each pleural lining is made up of mesothelial cells
* Small amount of fluid in pleural cavity reduces friction between lung and chest wall during breathing cycle
48
Explain the Diffusion Mechanisms of fluids in the lung and pluera
* Diffusion Mechanisms
* Hydrostatic pressure from parietal pleura drives fluid into pleural space
* Oncotic pressure from proteins in pleural space drive fluid into parietal/visceral spaces
* In normal conditions, the lymph system drains fluid in the pleural space
49
Pleuritis versus Pleuritic Chest Pain
define and give examples
* Pleuritis – pain due to inflammation
* Idiopathic, viral
* Pleurtic chest pain – sharp, stabbing, well localized pain exacerbated by inspirations (not necessarily having to do with the pleura)
* Rib fractures, PE, pneumonia
50
pleural effusions - what do you see on different modes of imaging
* Imaging
* Chest X-ray: see a meniscus of fluid line
* MRI – see fluid build-up in axial view
* Ultrasound – see expansion of pleural space
51
Chylothorax
description/etiology
* Pleural effusion due to damage to thoracic duct
* Chylothorax
* Description: Build-up of lymph fluid in the pleural space
* Etiology: Trauma, Malignancy
52
Transudates
examples/treatments
* Transudates – due to hydrostatic or oncotic pressure
* Examples:
* CHF – increase in hydrostatic pressure in pulmonary artery
* PE – increase in hydrostatic pressure in pulmonary artery
* Cirrhosis – liver produces less albumin à decreases in oncotic pressure
* Treat underlying problem
53
Exudates
examples/treatment
* Exudates – due to inflammation or disease of the pleura
* Examples:
* Pneumonia
* Parapneumonic effusion – exudate with uninfected fluid
* Empyema – infection of pleural space à formation of pus
* Tx: Surgical resections
* Malignancy, PE, GI disease
* Find underlying problem
54
Light criteria
transudates
* Transudates
* Pleural fluid protein : Serum protein \< 0.5
* Pleural fluid LDH : Serum LDH \< 0.6
55
Light criteria
exudates
* Exudates (ONLY need ONE of following)
* Pleural fluid protein : Serum protein \> 0.5
* Pleural fluid LDH : Serum LDH \> 0.6
* Pleural fluid LDH \> 2/3 upper limit of normal
56
Mesothelioma
description, signs/symptoms, prognosis, pathology
* Mesothelioma – associated with asbestos
* Signs & Symptoms: Dyspnea, chest pain
* Prognosis: poor, palliative care
* Pathology: black lung
57
Solitary fibrous tumor (SFT)
description, treatment
* Solitary fibrous tumor (SFT) – mesenchymal tumor from pleural surface
* Usually benign
* Become symptomatic when very large
* Treatment: surgical resection
58
Define ARDS
* A response to an injury (i.e. pneumonia, car accident, trauma) that causes a massive inflammatory response
* Cause of hypoxic respiratory failure
59
types of ARDS
* Types
* Pulmonary ARDS – due to direct lung injury (i.e. pneumonia, aspiration, inhalation, infection)
* Extrapulmonary ARDS – due to systemic processes (i.e. sepsis, pancreatitis, and trauma)
60
Criteris for ARDS
* Strict criteria for diagnosis
* Timing: less than 1 week following insult
* Imaging: bilateral opacities or infiltrates
* Origin of edema: infiltrates are not caused from heart failure (rule out via echo)
* Hypoxia: PF ratio \< 300
61
PF ratio
PF Ratio = PaO2 / FIO2 = 100/0.21 = 480 (that’s really good!)
62
What happens to VQ in ARDS?
* ARDS is caused by filling of alveoli with edema – unable to ventilate, leading to a V/Q ratio close to 0
63
Types of Hypoxemia (7)
how to diagnosis each
* ARDS – bilateral infiltrates on CXR
* Pneumonias – unilateral infiltrates on CXR
* Pulmonary embolism – clear on CXR
* CHF – BNP and echo findings
* Interstitial lung disease – chronic history of lung issues
* Pulmonary hypertension – no pulmonary infiltrates on CXR
64
two phases of ARDS
exudative, proliferative
65
What happens inthe exudative phase of ARDS
* Exudative Phase – flooding of proteinaceous fluid and edema
* Increased permeability (and cellular swelling) of alveolar membrane/capillary
* Hyaline membrane
66
What happens in the proliferative phase of ARDS
* Proliferative Phase – pulmonary fibrosis
* Stiff lungs due to interstitial fibrosis
* Less edema due to diuretics
* Progressive pulmonary HTN
* Interstitial inflammation (causing recruitment of fibroblasts)
67
What are the key features in each slide - how does it relate to ARDS
hyaline membrane
fibrosis
68
common complications of patients with ARDS (5)
* Stiff lungs
* Refractory hypoxia – neurological deficits
* Paralytics – myopathy
* Pyschological trauma
* ICU related-complication – HAP, ulcers, blood clots
69
explain PEEP and tidal volume treatment in ARDS
* PEEP (positive end expiratory pressure) – keeps alveolar sacs open
* Low tidal volume – reduces mortality
* Start patients at 8cc/kg
* Wean down patients to 6cc/kg
* Permissive hypercapnia – reduced inspiratory and expiratory phases à buildup of pCO2 à acidosis
70
What are some other treatment techniques used in ARDS (4)
* Prone position (flipping patient on face) – relieves distension of dorsal alveoli/decreases V/Q mismatch
* ECMO – acts as dialysis for the lungs
* Paralytics – reduce oxygen demand from body
* No steroids
71
Describe the prognosis for ARDS patients and the long-term sequelae of survivors of ARDS.
* Bad, 75% who survive will have some deficit
* High mortality rate
* High rate of PTSD
