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CardioResp > Week 9 > Flashcards

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
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2
Q

List some innate cell types.

A

Antimicrobial peptides, NK cells, phagocytic cells (macrophages, PMNs), dendritic cells

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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
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4
Q

What are NK cells?

A

NK Cells – kill virus infected cells

  • Resident cells
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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
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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
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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
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8
Q

In the alveolar space, where are the following located:

  • type I pneumocyte
  • type II pneumocyte
  • alveolar macrophage
A
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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
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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
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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
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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
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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
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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
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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
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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
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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
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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)
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19
Q

What type of infections are common with NK cell defects?

A

Viral infections

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20
Q

What kind of infections do you get with humoral cell defects?

A
  • Humoral defects = bacterial (especially encapsulated) infections
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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
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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
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23
Q

What are combined defects?

A
  • Combined defects = features of both humoral and cellular immunity
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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
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25
Q

Name 5 anti-histamines.

A

MNEMONIC ALERT (may or may not help): “_C_an’t _D_o _H_istamines _F_or _L_ife”

  • Cetirizine
  • Diphenhydramine
  • Hydroxyzine
  • Fexofenadine
  • Loratadine
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26
Q

What is the general mechanism of action of antihistamines?

A

Competitive H1 receptor (Gq receptor); although increase in intracellular Ca2+, histamine stimulation causes production of prostacyclin and NO, outweighing histamine’s vasoconstrictive effects

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27
Q

What are the uses of antihistamines?

What are the adverse effects of antihistamines?

A

Use: Allergy-mediated pathologies

Adverse Effects: Diphenhydramine and hydroxyzine have anticholinergic effects (aka sedating)

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28
Q

Name 2 decongestants

A
  • Pseudoephedrine
  • Phenylephrine
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29
Q

For decongestants (pseudophedrine, phenylepherine):

  • What is the MOA?
  • What are the uses?
  • What are some adverse effects?
A
  • MOA: Alpha 1 agonists (Gq) – vasoconstriction
  • Uses: Used to decrease mucus production
  • Adverse effects: Tissue necrosis if use extends past 3 days
30
Q

For intranasal corticosteroid:

  • Name one.
  • What is the MOA?
  • What is its use?
  • What are 3 adverse effects?
A
  • 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
Q

For expectorant:

  • Name one.
  • What is the MOA?
  • What is its use?
A
  • Guaifenesin
  • MOA: Increase respiratory tract fluid secretions and helps loosen phlegm
  • Use: Sinusitis (may help – “expect” it to help)
32
Q

For mucolytic agents:

  • Name one.
  • What is the MOA?
  • What is its use?
A
  • Example: acetylcysteine
  • MOA: Splits the disulfide linkages that holds mucus together
  • Use: Reduces sputum viscosity to improve secretion clearance
33
Q

For opioid antitussives:

  • Name three.
  • What are the MOAs?
  • What is its use?
  • Adverse effects?
A
  • 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
Q

For non-opioid antitussives:

  • Name one.
  • What is the MOA?
  • What is its use?
  • Adverse effects?
A
  • 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
Q

Define the following terms:

  • Nasopharyngitis
  • Acute rhinosinusitis
  • Acute otitis media
  • Acute infection pharyngitis
  • Rhinitis
A
  • 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
Q

What is the epidemiology of nasopharyngitis?

  • What age group does it most occur in?
  • How does transmission occur and what viruses?
A
  • 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
Q

What is the pathophysiology of nasopharyngitis?

  • What does yellow mucus mean? Green mucus?
  • What can bradykinin cause?
A
  • 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
Q

For nasopharyngitis:

  • What are the clinical symptoms associated with it?
  • Risk factors?
  • Complications as a result of the condition?
  • Diagnosis?
  • Treatment?
A
  • 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
Q

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?
A
  • 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
Q

What are the symptoms associated with acute rhinosinusitis? Differentiate between complicated and uncomplicated bacterial rhinosinusitis. How do you diagnose both?

A
  • 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
Q

What are two complications associated with acute rhinosinusitis? What are the treatments for the conditon (specifically for uncomplicated??)

A
  • 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
Q

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?
A
  • 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
Q

Discuss the pathophysiology of acute otitis media. What are the three bacteria involved?

A
  • 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
Q

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?
A
  • 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
Q

For acute infectious pharyngitis, indicate the symptoms associated with bacterial and viral?

A
  • Clinical
    • Bacterial
      • Age 5-15
      • Fever
      • White exudate on tonsils
      • Tonsillopharyngeal inflammation
      • Anterior cervical lymphadenopathy
    • Viral
      • Conjunctivitis
      • Hoarseness
46
Q

Distinguish between allergic rhinitis and non-allergic rhinitis.

A

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
Q

Define basic pleural anatomy

A
  • 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
Q

Explain the Diffusion Mechanisms of fluids in the lung and pluera

A
  • 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
Q

Pleuritis versus Pleuritic Chest Pain

define and give examples

A
  • 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
Q

pleural effusions - what do you see on different modes of imaging

A
  • 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
Q

Chylothorax

description/etiology

A
  • Pleural effusion due to damage to thoracic duct
    • Chylothorax
      • Description: Build-up of lymph fluid in the pleural space
      • Etiology: Trauma, Malignancy
52
Q

Transudates

examples/treatments

A
  • 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
Q

Exudates

examples/treatment

A
  • 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
Q

Light criteria

transudates

A
  • Transudates
    • Pleural fluid protein : Serum protein < 0.5
    • Pleural fluid LDH : Serum LDH < 0.6
55
Q

Light criteria

exudates

A
  • 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
Q

Mesothelioma

description, signs/symptoms, prognosis, pathology

A
  • Mesothelioma – associated with asbestos
    • Signs & Symptoms: Dyspnea, chest pain
    • Prognosis: poor, palliative care
    • Pathology: black lung
57
Q

Solitary fibrous tumor (SFT)

description, treatment

A
  • Solitary fibrous tumor (SFT) – mesenchymal tumor from pleural surface
    • Usually benign
    • Become symptomatic when very large
    • Treatment: surgical resection
58
Q

Define ARDS

A
  • A response to an injury (i.e. pneumonia, car accident, trauma) that causes a massive inflammatory response
  • Cause of hypoxic respiratory failure
59
Q

types of ARDS

A
  • 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
Q

Criteris for ARDS

A
  • 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
Q

PF ratio

A

PF Ratio = PaO2 / FIO2 = 100/0.21 = 480 (that’s really good!)

62
Q

What happens to VQ in ARDS?

A
  • ARDS is caused by filling of alveoli with edema – unable to ventilate, leading to a V/Q ratio close to 0
63
Q

Types of Hypoxemia (7)

how to diagnosis each

A
  • 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
Q

two phases of ARDS

A

exudative, proliferative

65
Q

What happens inthe exudative phase of ARDS

A
  • Exudative Phase – flooding of proteinaceous fluid and edema
    • Increased permeability (and cellular swelling) of alveolar membrane/capillary
    • Hyaline membrane
66
Q

What happens in the proliferative phase of ARDS

A
  • 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
Q

What are the key features in each slide - how does it relate to ARDS

A

hyaline membrane

fibrosis

68
Q

common complications of patients with ARDS (5)

A
  • Stiff lungs
  • Refractory hypoxia – neurological deficits
  • Paralytics – myopathy
  • Pyschological trauma
  • ICU related-complication – HAP, ulcers, blood clots
69
Q

explain PEEP and tidal volume treatment in ARDS

A
  • 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
Q

What are some other treatment techniques used in ARDS (4)

A
  • 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
Q

Describe the prognosis for ARDS patients and the long-term sequelae of survivors of ARDS.

A
  • Bad, 75% who survive will have some deficit
  • High mortality rate
  • High rate of PTSD

CardioResp (14 decks)

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