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Conj 403 > Midterm 2: Rachael > Flashcards

Midterm 2: Rachael Flashcards

1
Q

Functions of Respiratory System

A
  1. Blood Gases
  2. ECF
  3. Other
    • Removes clots
    • Speech
    • Blow, sucking
    • Valsalva maneuver
    • Sobbing, laughing, yawning
    • Ion Transport
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2
Q

pH ECF: Overview

A
  • Carbonic anhydrase
  • Increase in CO2: Respiratory acidosis
  • Decrease in CO2: Respiratory alkalosis
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3
Q

Flow of Air through Large Airways

A
  • Nasal pasage
  • Pharynx
  • Larynx
  • Trachea
  • Primary bronchus
  • Secondary bronchus
  • Through 10 branchings
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4
Q

Nasal Passages

A
  • Moisten, warm and clean air
  • Conchae increase surface area
  • Conchae create turbulence to create more air-epithelium contact
  • Little energy to breathe at sea level
  • Cilia to move particles to pharynx
  • (Sinuses lighten the skull)
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5
Q

Pharynx

A
  • Nasopharynx, oropharynx, laryngopharynx
  • Substantial MALT
    • Tonsils
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6
Q

Larynx

A
  • Blocked during swallowing by the epiglottis
    • larynx being pulled up and forward under the mandible
    • back of the tongue is being pushed backward.
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7
Q

Trachea

A
  • hemicircular cartilage bands
    • posterior is flexible
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8
Q

Bronchi

A
  • larger bronchi, similar structure to the trachea
  • smaller bronchi, the cartilage is in the form of plates
  • smooth muscle and submucosal glands
  • Ten branches
  • Narrowest parts are bronchi
    • Larger points can have role in constricting airflow
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9
Q

Advantage of posterior trachae being flexible?

A
  • Coughing
  • Epiglottis is closed, increasing intrapleural pressure
  • Pushes in the posterior, creating higher air velocities
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10
Q

Bronchioles

A
  • Airway without cartilage
  • Terminal bronchioles:
    • Smooth muscle
    • Only airway epithelium
  • Respiratory bronchioles
    • Alveoli branch off
    • Cuboidal epithelium
    • No cilia
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11
Q

Alveolar Ducts

A
  • No airway epithelium
  • Structure is from alveoli
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12
Q

CT scan of Upper Lung Lobes

A
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13
Q

CT scan of Lower Lobes

A
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14
Q
A
  • pulmonary angiogram
    • ​ radio-opaque dye was injected from a catheter into the right pulmonary artery
  • branching of the pulmonary artery follows the branching of the bronchi
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15
Q
A
  • No cartilage=bronchioles
  • Those without alveoli=terminal bronchioles
  • TB lead into repspiratory bronchioles which have thin walled alveoli branching off of them
  • Open space leading to alveoli is alveolar duct
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16
Q

Airway Epithelium

A
  • Ciliated
  • Pseudostratified, simple columnar ciliated epithelium
  • Basal cells regenerate the other cells
  • Goblet cells release mucus
  • Submucosal glands releasing mucus and fluids
    • Acinar
      • Both mucus and serous
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17
Q

Regulation of Airway Smooth Muscle

A
  • Parasympathetic nerves: contraction of the smooth muscle.
  • Sympathetic nerves: relaxation/dilation of smooth muscle
    • Beta receptors
  • Inflammatory paracrines: contraction. Histamine
    • PLA2: Arachadonic derivative giving rise to leuoktrienes. Therefore no NSAID for asthma
  • Increased carbon dioxide leads to dilation. Increases airflow.
    • Also matches the two sides of the lung
  • Neural reflexes through sensory afferents. Stimulates parasympathetic neurons/constriction. Irritating stimuli or inflammation.
    • Locally or through CNS
  • Epinephrine pops airways open
    *
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18
Q

What substance is cleaved from a membrane phospholipid by phospholipase A2? Then, what enzyme acts on this substance to begin the synthesis of leukotrienes?

A

Phospolipase A2 acts on a membrane phospholipid to cleave off arachidonic acid. In the pathway leading to leukotrienes, the enzyme that acts on the arachidonic acid is lipoxygenase.

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19
Q

Regulation of Submucosal Glands

A
  • Parasympathetic nerves cause secretion. Stimulation of sensory afferents by irritant or inflammation. CNS or locally.
    • Block this in surgery to prevent extra secretions
  • (Sympathetic effects are rather weak, with alpha1 adrenergic inhibiting secretion and beta2 stimulating secretion.)
  • Inflammatory paracrines stimulate secretion.
  • Neural reflexes occur starting with stimulation of sensory afferents in the airways, which can lead to stimulation of parasympathetic neurons.
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20
Q

Fluid Transport in Epithelium

A
  • More ions, more water through osmosis into mucus
    • net movement of chloride ions from the interstitial fluid into the lumen
  • From interstitial fluid: Chloride, potassium and sodium cotransporter
  • Chloride ions enter the lumen via a regulated chloride channel
    • second messenger, cyclic AMP, activates a kinase that phosphorylates the chloride channel, which leads to its opening.
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21
Q

Alveolar Cells

A
  • Type I
  • Type II
  • Capillary Endothelial Cells:
  • Fibroblasts
  • Macrophages
  • Neutrophils
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22
Q

Type I Cell

A
  • Cell immediately bordering inhaled gas
  • Very thin
  • Cells that oxygen and carbon dioxide diffuses through
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23
Q

Type II Cell

A
  • If damage type 1 cell with connective tissue in tact, can divide and replace type 1
  • Release surfactant, reduce the surface tension
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24
Q

Capillary Endothelial Cells

A
  • Thin: combination of the type I cells and endothelial cells are less than 0.5 um
  • 0.2 micrometer
  • Very smallest thing you can see on a light microscope
  • That is all that gas has to diffuse across
  • Lots of capillaries and cover a lot of alveoli wall
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25
Q

Fibroblasts

A
  • found in and form the interstitium
  • factors can stimulate these abnormally, leading to fibrosis and thus restrictive lung disease
  • Has elastin:
    • Too much elastin causes fibrosis
    • Compliance of lungs go down
    • Restrictive lung disease
    • Breaks down, ephysema
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26
Q

Macrophages

A
  • Slow turn over
  • Go up and get swept away
  • Infection, abnormal macrophage number
  • Releasing proteases and oxygen radicals
  • enter the alveoli from the blood and leave via the mucus in the airways
  • Release protective anti-protease so don’t degrade themselves
  • Lots of inflammatory paracrine release leading to a cytokine storm
    • Fatal
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27
Q

Neutrophils

A
  • join the resident macrophages in an acute lung infection
  • Neutrophil elastase, sloppy eaters, can cause damage
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28
Q

Role of Surfactant

A
  • yellow layer shown covering the type I cells is a thin layer of fluid
    • Necessary since they are living cells
    • If normal fluid, pressure would collapse lungs
  • Surfactant secreted by Type II cells
  • 80-90% phospholipid, plus four special amphipathic proteins
29
Q

Surface Tension vs. Area Graph

A
  • surface tension in a surface of pure water is the same at all areas
  • Detergent reduces surface tension and the same at all areas
  • Surfactant extracted from lungs is added to water
    • Greatly reduces surface tension and has a strong effect of area
  • Small areas have the surface tension reduced much more than large areas.
    • Small alveoli have less surface tension than larger alveolis
30
Q

why having less surface tension in small alveoli would be helpful and would reduce the work of breathing.

A

Alveoli are small at the beginning of an inhalation. This is exactly when you would want alveoli to expand easily. Then during the inhalation the surface tension increases until it is substantially higher just before the exhalation.

31
Q

Think back to the Law of Laplace (discussed under “Heart Failure”). If alveoli did not have surfactant and thus alveoli of two different sizes had the same surface tension, how would you expect the pressure in the smaller alveolus to compare to the larger?

A

The pressure would be GREATER in the smaller alveolus.

32
Q

infant respiratory distress syndrome.

A
  • Happens in premature babies
  • Lungs are the last things to develop
    • surfactant last substance synthesized
  • Premie might not have enough surfactant
    • Too stiff
    • Not enough compliance to inhale, grunt at exhalation because air comes out fast
  • Alveoli collapse
  • Positive pressure respirator (not good for long term)
  • Animal surfactant
  • tachypnea (fast breathing) and cyanosis (blue)
33
Q

Total Lung Capacity

A
  • Following a maximum inhalation, the amount of gas in your lungs
  • 5.9 L for a 150 lb person
34
Q

Forced Vital Capacity

A
  • Following this maximum inhalation, the maximum amount of gas you can then exhale
  • 4.7 L in 150 lb person
35
Q

FEV1

A
  • Following a maximum inhalation, this is the maximum amount you can exhale in the first second
  • often expressed as a percentage of the forced vital capacity
36
Q

Residual Volume

A
  • Following a maximum exhalation, there is necessarily some gas left in your lung
  • 1.2 L in 150 lb person
37
Q

Functional Residual Capacity

A
  • amount of gas in your lungs following a normal exhalation
  • Changes in respiratory diseases like COPD and asthma
  • 2.4 L in 150 lb person
38
Q

Alveolar Ventilation

A
  • amount of new air entering someone’s alveoli per minute
  • VA=(VT-VDS)f

Alveolar volume, tidal volume, dead space volume

39
Q

Tidal Volume

A
  • it is the amount being inhaled and exhaled at any given time.
  • First gas to alveoli is always last exhaled gas
    • alveolar gas
40
Q

anatomical dead space

A
  • Gas in airways
  • volume in milliliters is approximately equal to a person’s weight in pounds
  • This amount must be substracted from the tidal volume to get the amount of new air entering the alveoli on each breath.
41
Q

alveolar dead space

A
  • volume in any alveoli that are not being perfused with blood
  • Normally insignificant but can become significant is some disorders.
42
Q

Atelectasis

A
  • Collapsed lung
  • Gap opens in pleural space
  • Improper inflation
    • depends on the tight attachment of the visceral and parietal pleura
43
Q

Atelectasis Treatments

A
  • If seperation not too large, may resolve on its own
  • positive pressure ventilator
  • large syringe and needle might be used to withdraw gas from the space
  • chest tube
    • valve that lets gas leave but not enter pleural space
44
Q

Obstructive Atelectasis

A
  • clogged bronchus
    • tumor, mucus
  • distal to the blockage
    • oxygencontinually removed from the alveoli by the blood flowing through the pulmonary capillaries
  • RBC in capillaries bind oxygen
  • This lowers pressure in alveoli
45
Q

Absorptive Atelectasis

A
  • linked to obstructive atelectasis
  • breathing supplemental oxygen
  • more gas is removed from the alveoli and the pressures decreases more
46
Q

Pneumothorax

A
  • air or gas in the intrapleural space
  • wound that punctures the chest wall
    • “sucking chest wound”
      • inhalation causes air to flow through the wound into the intrapleural space
    • Put paper over wound
  • Lung infection (TB)
    • seriously damaged airways, allowing air to flow from a bronchus into the intrapleural space.
  • emphysema
    • Lung tissue destroyed
    • especially likely if bullae are present
  • Spontaneous
    • tall, thin young man
47
Q

Surfactant Problem

A
  • surfactant is secreted by type II alveolar cells and acts to reduce the surface tension in alveoli
  • Can causes atelectasis
48
Q

ARDS

A
  • disorder of epithelial inflammation
  • Acute (NOT adult only)
  • Can be fatal
  • In severe respiratory infections (fatal influenzas)
  • Trauma, 12-24 hours after
  • Sepsis
49
Q

ARDS causes

A
  • serious infection such as pneumonia
  • dangerous influenza A
  • severely damaged by inhalation of stomach contents or a toxic gas
  • Severe trauma involving shock and transfusions
  • Sepsis is the presence of pathenogenic microorganisms or their toxins in the blood accompanied by a subsequent systemic inflammatory response
50
Q

ARDS characteristics

A
  • dyspnea signals the onset of serious problem
  • hypoxemia: blood not oxygenated enough
  • hypercapnia: carbon dioxide not blown off fast enough
  • Normal PaO2 is 100mmHg, ards is 40
  • protein-rich infiltrates accumulating in the alveoli
  • not due to high pulmonary venous pressure, but to changes occuring in the epithelia in the alveoli.
51
Q

ARDS pathology

A
  • neutrophils enter alveoli joining naturally present macrophages
  • Important for dealing with issue but also escalate ARDS
  • Inflammatory paracrines and cytokines
  • Leaky epithelium
  • type I cells likely are dying, with the type II cells unable to replace them fast enough
    • surfactant problems
  • fluid-filled alveoli poorly oxygenate the blood, supplemental oxygen not help here
  • substantial fibrosis in the extracellular matrix
52
Q

ARDS Resolution

A
  • two thirds of the patients eventually resolve the difficulties
    • neutrophil apoptosis and macrophages clean up mess
  • Fibrosis may be repaired
  • one-third of the total, the lungs become heavy and virtually without air
    • fatal
53
Q
  • Patient D
  • Is it normal for asthma to be mild?
  • What is albuterol?
  • Is there nonetheless a way in this patient to test for a tendency for asthma in spirometry?
  • Is his medication adequate?
  • Next step to control asthma?
  • What would be done if his asthma moved up to moderate persistent?
A
  • Mild asthma is common
  • Albuterol= inhaled, short acting beta agonist
  • methacholine challenge to see if the airways are hyper-responsive. Methacholine is a muscarinic, cholinergic agonist.
  • Not controlled because wheezing with sleep and wheezing after tennis. Only on rescue inhaler.
  • low dose, inhaled glucocorticoid, (maybe leukotriene receptor antagonist) to control asthma
  • Moderate-persistant: inhaled, long acting beta agonist such as salmeterol. But another possibility is to increase the dose of the glucocorticoid. Another option is to add a leukotriene modifier to the inhaled glucocorticoid.
54
Q
  • Patient E
  • What is the significance of the skin testing for allergens and the measurement of the serum IgE level?
  • Does omalizumab inactivate plasma IgE, IgE bound to mast cells, or both?
  • Is there another possibility if they decide not to use omalizumab?
A
  • considering the addition of an expensive, additional drug, omalizumab. This monoclonal antibody binds to the Fc region of IgE. This drug only is used with moderate to severe asthma, which is not under control
  • Only plasma IgE because binds Fc region
  • leukotriene modifier could be added as a third drug,
55
Q
  • Patient F
  • When is an inhaled cholinergic antagonist used in asthma?
  • What are here lab values like?
  • pH=7.7
  • PaO2=what hemoglobin binding
  • What happened?
A
  • Not usually as daily therapy, except under unusual circumstances. For example, perhaps a patient cannot use inhaled beta agonists. In emergency departments, it may be added to inhaled beta agonists, as in this case.
  • Oxygen below normal and so is carbon dioxide (CO2 says ventilation greater than normal)
  • Respiratory alkalosis
  • 80%
  • Asthma attack progressed so couldn’t blow off CO2. O2 also fallen further
56
Q

Asthma Epidemiology

A
  • prevalence, which is the number of cases in the specific population at a specific time
  • Higher prevalence in boys
    • Tend to outgrow asthma
  • Girls have reduced prevalence of asthma, comes on in young adults
    • women more likely severe group
  • Racial, ethnic, rural/urban,
  • Obesity (but is it obesity or lack of exercise)
  • Obstructive disease; trouble getting air into the alveoli
  • Alveoli are okay
  • Reversible
  • Given albuterol, beta-2-agonist and measure FEV1 (forced exhalation volume) again and see if improve; diagnostic of asthma
57
Q

What is asthma

A
  • inflammation leading to airway hyper-responsiveness
  • contraction of the smooth muscle, edema and mucous secretion
  • Reversible
58
Q

Atopic Asthma

A
  • genetic predisposition and environmental factors
  • TH2 cells
  • B cells release cytokines favoring IgE
  • Allergen or precipitating factor lead to exacerbation
59
Q

Non-Atopic Asthma

A
  • stimulation of the airways by a non-antigenic factor
    • exercise, cold air, tobacco
  • IgE not a factor
  • afferent neurons are stimulated
  • reflex (locally or via the CNS) that leads to contraction of smooth muscle and secretion by submucosal glands
60
Q

Sequence of Asthma

A
  • First phase
    • In first hour
    • Mast cells release inflammatory paracrine
      • histamine, leukotrine
    • contraction of smooth muscle, edema in all layers of airway wall, mucus secretion
  • Second Phase
    • 4-6 hours
    • Cytokines
    • Infiltration of cells
    • Hyperresonsive
  • Third Phase
    • Weeks to months
    • Airways remodeling
    • walls of the airways thicken, with more submucosal tissue, including capillaries
    • basement membrane of the epithelium thickens
    • goblet cell hyperplasia
61
Q

Causes of Atopy

A
  • set of antigens the immune system is exposed to in infancy determines whether or not a genetically predetermined individual tends to develop atopic responses.
  • TH2 triggers lots of inflammation because thinks it is a worm. TH1 is more antibody oriented
62
Q

what factors lead to a a patient winding up in an emergency room with a severe exacerbation?

A
  • Usually atopic response
  • Non-atopic factors can contribute
  • With asthma, other factors can exacerbate
    • viral infection
  • Three separate issues:
    • Allergens
    • Atopy cirumstances
    • Other factors that make asthma worse
63
Q

Asthma Treatments

A
  • inhaled, short-acting beta2 agonist
  • inhaled corticosteroid
  • inhaled, long-acting beta2 agonist
  • leukotriene receptor antagonist
  • anti-IgE monoclonal antibody
64
Q

inhaled, short-acting beta2 agonist: for asthma

A
  • albueterol
  • begins in five minutes and persists for 30 to 60 minutes
  • more than two days per week or more than twice a month following a nighttime awakening…switch to next step
65
Q

inhaled corticosteroid: for asthma

A
  • fluticasone
  • supress inflammation, infiltration of cells and mucosal and submucosal changes
  • dose is increased if the initial dosage is not adequate
  • side effects at high doses
66
Q

inhaled, long-acting beta2 agonist

A
  • salmeterol
  • work for 12 hours or so
  • always with corticosteroid
  • PO is contraindicated
67
Q

leukotriene receptor antagonist

blocker of lipoxygenase

A
  • leukotriene receptor antagonist: monteleukast
  • blocker of lipoxygenase: zileuton
  • few hours to have an effect and reach their maximum action in a couple of day
  • Instead of corticosteroids for rhinoconjunctivis
68
Q

anti-IgE monoclonal antibody

A
  • omalizumab
  • every two or four weeks
  • Binds Fc regions of antibody
  • skin test and serum IgE measurements done
69
Q
A

Conj 403 (7 decks)

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