Patho/ Pharm Exam 3

Front 1

What is Cilia?

Back 1

- Conical tip/tapered basal root
•Moving things out, the primary defense of the nasobroncho tree
•Used to be called the Na+ H2O escalator
•Moves mucus along where it is anatomically supposed to go
•Destroyed by heat, lack of moisture, trauma, and hypernatremia
•Figure 21-4 pg. 512

Front 2

What are goblet cells and how much mucus do they produce?

Back 2

- Produce 100 mL/day of mucus
•Children have more Goblet cells= more obstructions
o So full of mucus, they push the nucleus down to the bottom

Front 3

What are Paranasal sinuses and its 4 functions?

Back 3

1. Speech resonance
2. increase Heat vapor
3. increase Water Vapor
4. Exchange Surface
• Have space, heat up the air that goes into the lungs

Front 4

What is the Eustachian tube?

Back 4

- Shorter in children potential for Otitis media
•Important in peds with chronic ear infections -> Know how it connects with the pharynx (peids only)
o Close the mouth, pinch the nose --> can blow out the tempatic membrane

Front 5

What is the Serous Gland?

Back 5

- Secretes serous fluid, necessary for the structures to stay moist

Front 6

What is Carina and what does it contain?

Back 6

- Contains majority of cough receptors. Point of two main stem bronchi
• When giving someone an endotracheal tube, make sure not to put it all the way down to the carina because it will block and cut off the airway

Front 7

Where is Cartilage found in the airway?

Back 7

Only resent in the trachea; delicate tissue

Front 8

How long does it take until the lungs are completely developed?

Back 8

Lungs fully developed by 8 years

Front 9

How long does it take until premature lungs are completely developed?

Back 9

- Premies are born with a lot of problems but their muscles will grow massive
- We worry about an obstruction until they are 8 years old due to the amount of Goblet Cells
o They have more Goblet Cells than adults --> new cells, very responsive

Front 10

What is the number of alveoli in Adults, Newborn, and Premature infants?

Back 10

- Adult- 300 mil
- Newborn- 4 mil
- Premies- do not have the surfactant they need to have in order to have alveolar function

Front 11

How do Chemoreceptors help with respiration?

Back 11

- Central chemoreceptors (medullary center) respond to CO2 and pH changes.
- Small increase in PaCO2 causes normal stimulus to breathe.

Front 12

What drives respiration?

Back 12

- The medulla is driven by amount of CO2
- When pathologies cause difficulty removing CO2, the body becomes accustomed to low CO2 (pathological)

Front 13

What is PaCO2?

Back 13

- Partial pressure of CO2

Front 14

What happens when there is an abnormal increase in PaCO2?

Back 14

- PaCO2 can stimulate a 10 fold increase in Alveolar ventilation

Front 15

What happens when there is a decrease in pH?

Back 15

- Acidosis which can increase Alveolar respiration by receptors in the aortic arch and carotid bodies
- Adjustments will be made in both acidic and alkalotic environments.

Front 16

What are proprioreceptors and their functions?

Back 16

- Muscle and joint movement
- Sensory nerve stimulation
- CNS (Rate and depth of breaths adjusted to demand by B/P)

Front 17

What are Baroreceptors and their functions and where are they located?

Back 17

- Aortic Arch (vagus nerve)
- Carotid Bodies (glossopharyngeal nerve)
- Increase in B/P --> Decrease in Respiration
- Sitting still, no reason to be breathing fast
- Decrease in B/P --> Increase in Respiration
- Usually means person may be in a shocked state

Front 18

What are the 5 ways a brain can cause an interruption of Alveolar CNS stimulation?

Back 18

1. Head trauma
2. Stroke
3. Tumor: Neuroplasia
4. Drugs: Causes sedations
5. Infection: Toxins being released

Front 19

What are the two ways a spinal cord cann cause an interruption of Alveolar CNS stimulation?

Back 19

1. Nerves: Enervation of respiratory muscles; trauma, tumor, polio, myasthenia gravis, Lou Geriigh's Disease, MS (multiple sclerosis), MD (muscular distrophy) infection
2. High injury in the spinal cord and other diseases: interruption in the pathway
- Be sure to note the rate and depth of respiration will tell you how the pt. is compensating and how the pathology is taking over
- Depth can be the problem because it can steal CO2

Front 20

What is the second process of respiration?

Back 20

Perfusion: circulating the blood through the capillary bed

Front 21

What are the four Perfusion requirements?

Back 21

1. Adequate blood volume
2. Adequate hemoglobin (not anemic)
3. Intact, non-occluded capillary bed
- An occluded capillary bed occurs because edema is near it and close the capillaries easily
4. Functioning left heart
- Pumping blood carrying O2 throughout the body

Front 22

What is the difference between Perfusion and Saturation?

Back 22

Perfusion: How distributed the blood is
- Tested by Capillary refill: normal is 3 sec
- All four perfusion requirements are needed
Saturation: How much O2 there is

Front 23

What are the 2 problems associated with low hemoglobin concentration and what do they depend on?

Back 23

1. Anemia
2. Fe deficiency
3. Blood volume (needed) depends on the reaction of the body that causes the body to go into shock

Front 24

What is the most important factor in combining ventilation and perfusion via V/Q?

Back 24

- The matching of adequate *volume of air in the alveoli (4L/min) to adequate pulmonary blood flow (5L/min)
- Normal V/Q matching = 0.8

Front 25

What is normal V/Q matching?

Back 25

- Normal V/Q matching is 0.8
- The closer the number is to 1 the better the ratio

Front 26

What four cases would there be a V/Q mismatch?

Back 26

- Mismatch occurs in
1. Dead space
2. Shunt: "removed" anything that creates an area that cannot be used
3. Pulmonary embolism (PE): Clot shutting off the volume of air--> must be removed surgically
4. Atelectasis
- Occurs when a person has problems breathing

Front 27

What is a V/Q match?

Back 27

- Matching the adequate volume of the alveoli to the blood flow
- The 1/3rd of the alveoli that is in reserve

Front 28

What are the V and Q in the V/Q match?

Back 28

V= Volume of air in the alveoli
Q= Pulmonary Blood Flow
- 1/3rd of he lungs held in reserve
- Has to do with ventilation and constriction
- Pulmonary capillary is being compressed by edema and unable to preform O2 exchange

Front 29

What four ways does respiratory function effect the cell?

Back 29

- Hydrogen ions decrease pH (more acidic) effecting:
1. Speed of cellular reaction
2. Cell function
3. Cell Permeability
4. The very integrity of the cell

Front 30

How many O2 molecules do each hemoglobin carry and how does saturation levels effect the transportation?

Back 30

- Each hemoglobin molecule carries 4 molecules of O2
- The more saturated the hemoglobin is the closer it gets to concentration and the easier it becomes for the hemoglobin to let go of the O2 molecule --> Perfusion
- Eventually it will become harder for the RBC to let go again

Front 31

What is the essential component of the Citric acid cycle?

Back 31

- O2
- We breathe in O2 so the mitochondria can make ATP

Front 32

What can stop O2 from reaching the mitochondria and therefore stops the creation of ATP?

Back 32

Pathology

Front 33

What is the #1 characteristic of the pulmonary system?

Back 33

- It is continuous, has no borders or barriers

Front 34

Being that the pulmonary system is continuous, how can this cause a problem?

Back 34

- A microbe can affect a single area but the inflammatory response will affect multiple areas
- The whole lung is then affected by the action that happens in 1 lobe.

Front 35

How do structures involved in gas exchange differ from conducting structures?

Back 35

- The trachea, bronchi, and bronchioles serve as conducting passage ways for air, and do not engage in gas exchange
- Exchange in respiratory gases occurs in the alveoli that have a grapelike structure which provides a huge surface area for gas exchange (514-516)

Front 36

What are the 3 factors that determine breathing?

Back 36

1. Lung compliance
2. Airway resistance (diameter of the airways)
3. Opposing lung forces (elastic recoil vs. chest wall expansion)
(521-524)

Front 37

How are O2 and CO2 transported in the circulation?

Back 37

- O2 is transported in the blood primarily through binding to hemoglobin, and less so as dissolved in solution.
- CO2 is transported in the blood most importantly as the bicarbonate ion, dissolved or as carbaminohemoglobin (pgs. 527-528).

Front 38

What are the 2 factors that affect the distribution of ventilation and perfusion in the lungs?

Back 38

1.Body position affects the distribution of ventilation, with ventilation being higher in the bottom of the lung and decreased toward the apices when in an upright position.
2. Distribution of blood flow is affected by gravity such that perfusion is greatest in dependent lung fields (in the bases) (pgs. 522-526).

Front 39

How are alveolar ventilation and oxygenation estimated and assessed?

Back 39

- Estimated by: calculating the alveolar ventilation
- Alveolar ventilation (VA)= [Tidal volume (VT) - Dead space volume (VD)] x [Respiratory rate (RR)]
- VA = (VT-VD) x RR
- Oxygenation can be assessed by calculating the difference between alveolar and arterial oxygen tensions (A – aDO2), with a large value indicating poor matching of alveolar ventilation with alveolar blood flow. (520-521)

Front 40

What are the risk factors of Pulmonary Venous Thromboembolism (PE) there are 7 and Hyertension (HTN), there are 5?

Back 40

Risk factors of PE:
1. Venous stasis/sluggish blood flow
2. Hypercoagulability
3. Damage to the venous wall; complications include:
3a: right-sided heart failure
3b. hypotension
3c. pulmonary infarction
3d. necrosis.
Risk factors of HTN:
1. portal hypertension associated with cirrhosis
2. use of appetite-suppressant drugs
3. HIV infection, or the presence of mechanisms that increase pulmonary vascular resistance
4. left atrial pressure, or pulmonary blood blow/viscosity.
Complications of HTN include:
5. cor pulmonale
6. right ventricular failure

Front 41

What are the 4 types of malignancies?

Back 41

1. Squamous Cell Carcinoma
2. Adenocarcinoma
3. Large cell Carcinomas
4. Small cell carcinomas
(535-56)

Front 42

What are the 4 common causes of acute airway obstruction?

Back 42

1. exposure to allergens
2. exercise, stress
3. exposure to pulmonary irritants
4. occupational allergens

Front 43

What is the role of inflammation in the development of asthma?

Back 43

- Allergic (extrinsic) asthma is mediated by IgE, which is produced in response to specific antigens.
-The IgE binds to mast cells and causes them to release inflammatory chemicals in response to antigen (pgs. 541-542).

Front 44

What are the pulmonary function test?

Back 44

1. a decreased FEV1
2. low FEV1/FVC ratio (<70%)
3. improvement in FEV1 after use of a bronchodilator 4. increased residual volume
5. increased functional residual capacity
(pgs. 559-561).

Front 45

What are the 5 common signs/symptoms of acute airway obstruction?

Back 45

1. wheezing
2. feelings of tightness in the chest
3. dyspnea
4. cough
5. increased sputum production.

Front 46

What are the 8 severe signs/symptoms of acute airway obstruction?

Back 46

1. Expiratory and inspiratory wheezing
2. tachycardia,
3. tachypnea
4. use of accessory muscles of respiration
5. intercostal retractions
6. orthopnea
7. agitation
8. cyanosis

Front 47

What is a B2 agonist used for?

Back 47

-inhibit bronchial smooth muscle cell contraction, mucosal edema and mucus secretion

Front 48

What is an Acetylcholine antagonist used for?

Back 48

- decrease parasympathetic nervous system stimulation of mast cells
- Aids in drying up excessive mucus
- Used in chronic bronchitis, emphysema, and adjacent therapy for asthma
- Blocks muscarinic receptors to achieve bronchdilation --> tachycardia

Front 49

What are leukotriene inhibitors used for?

Back 49

- block the release of histamine, leukotrienes, and prostaglandins from the mast cells

Front 50

What are corticosteroids used for?

Back 50

- inhibit bronchial smooth muscle cell contraction, mucosal edema and mucus secretion
- block chemotaxis of neutrophils and eosinophils and mast cell degranulation

Front 51

What are mast cell stabilizers used for?

Back 51

- block antigenic and nonantigenic stimuli that cause mast cell degranulation

Front 52

What are the 5 classes of drugs used to decrease inflammation?

Back 52

1. B2 agonists
2. acetylcholine antagonists
3. leukotriene inhibitors
4. corticosteroids
5. mast cell stabilizers

Front 53

What are the 4 characteristics of Asthma?

Back 53

1. Parasympathetic --> CES
2. First presents itself in childhood
3. Presents itself in adulthood due to exposure of new toxins
4. A chronic obstructive pulmonary disease that presents suddenly

Front 54

What are the 3 manifestations of asthma?

Back 54

1. Constriction: of broncho smooth muscles
2. Edema: IgE and Mast cell degradation
3. Secretion: Initially dry cough --> then tenacious mucus but scant

Front 55

What are the 5 causes of acute exacerbations?

Back 55

1. Allergens: IgE mediated response
1a. Inability to run
2. Cold Air
3. Irritants: Smoke, Pollen
4. Medications: Aspirin, Ibuprofen, Advil
4a. We don't know why medications cause the airway to constrict
5. Chronic Obstruction worsened by asthma

Front 56

What are the 3 retractions and where are they located?

Back 56

1. Supraclavicular: Above or below the clavicle (occur during an asthma attack)
2. Substernal: 2nd worse
3. Intercostal retractions: most severe

Front 57

What are the 9 signs and symptoms of a person having an asthma attack?

Back 57

1. Wheezing
2. Nonproductive cough
3. Dyspnea: Different way of breathing
4. Tachypenea (fast breathing)
5. Retractions r/t small airway constriction
6. Tachycardia: An early sign of Hypoxemia
7. Cynosis: Late sign --> an emergency
8. Seesar respirations: Stomach then chest rises (ok only in pediatrics
9. Tripod position

Front 58

What are the 3 characteristics of Phase 1 in Asthma pathogenesis?

Back 58

1. Release of histamine
2. Bronchoconstriction and bronchial edema
3. Usually will respond to Beta 2 agonist

Front 59

What are the characteristics of phase 2 in Asthma pathogenesis?

Back 59

1. WBC invade bronchioles causing edema and swelling of bronchioles
2. Pt. will tripot to help support diaphragm as high as possible
3. May need steroids to get fluid out of lymph system
- Will not respond to Beta agonists
4. Hyperressonance: noise heard all over chest
5. Disphonia: pts should always be able to talk
6. Correct hypoxia by reversing the bronchospasm
7. Treat the inflammatory process

Front 60

What is status asthmaticus?

Back 60

- A severe, prolonged asthma attack which does not respond well to usual treatment
- Bronchodilators dont work
- There may be a silent chest --> no air movement
- Acidosis --> blood gas taken using a large bore IV
- May have to incubate (in controlled environment)

Front 61

What are the 2 types of COPD and their manifestations?

Back 61

1. Emphysema --> Alveoli
2. Chronic bronchitis --> bronchi

Front 62

What are the 4 causes of chronic bronchitis and what is the common name of someone with chronic bronchitis?

Back 62

1. Smoking
2. Hypersecretion of mucus and a productive cough for 3 months a year for 2 years
3. Increased sticky mucus: enables bacteria to stick around and its good for bacteria to grow and thrive because its a productive cough
- Name is a Blue Bloater
4. can lead to an airway obsruction

Front 63

What are the 5 signs and symptoms of chronic bronchitis?

Back 63

1. Decreased exercise tolerance due to the inability to breathe
2. Cough --> productive
3. Wheezing, SOB (shortness of breath)
4. Hypoxic and retention of CO2
5. Frequent pulmonary infections

Front 64

What are the 4 causes of Emphysema and what is the name of someone with Emphysema?

Back 64

1. Smoking
2. Permanent enlargement of alveoli with destruction of the alveoli walls --> inability to accommodate
3. Loss of elastic recoil: increased compliance
4. Bacterial infections increase destruction due to lack of inhibition of the proteolytic enzyme
- Called Pink Puffers because of the use of accessory muscles and pursed lip breathing

Front 65

What are the 7 signs and symptoms of Emphysema (dry)?

Back 65

1. Dyspnea that progresses and is measurable
2. Cough: scant sputum
3. Tachypnia
4. Prolonged expanding phase --> no constriction
5. Tripod position to increase lung capacity
6. Thin, catchexic: due to the inability to breathe while eating
7. Alveoli
- Thick walls
- Capillary closing pressure: leads to low O2

Front 66

What is dyspnea?

Back 66

Difficulty breathing

Front 67

What is Bronietasis?

Back 67

- An infection with PUS working to get the infection out due to a dilation of the bronchi
- 50% of cases are associated with cystic fibrosis (children at higher risk)

Front 68

What is the pathogenesis of Bronietasis?

Back 68

- Infection, inflammation, destructive process that leads to pus formation

Front 69

What is the clinical manifestation of bronietasis?

Back 69

- Productive foul smelling cough-tri layer (abscess or pus)
- Clubbing, fever, night sweats

Front 70

What are the 4 treatment of bronietasis?

Back 70

- ABX
- Bronchiodilators
- Chest CPT (physiotherapy)
- Chest percussion

Front 71

What is the pathogenesis of Bronchiolitis?

Back 71

- Proliferation and necrosis of bronchiolar epithelium
- Widespread inflammation of bronchioles (RSV) Respiratory Surgintal Virus = 50% of cases
- Caused by airway obstruction, atelectasis, and hyperinflation
- Increased O2 saturation
- Occurs in the terminal end of the bronchioles --> near the alveoli

Front 72

What are the clinical manifestations of Bronchiolitis?

Back 72

1. Wheezing
- Wheezing occurs because it does not stay in one area
2. Dysnpea
3. Techycardia
4. Retractions
5. Otitis Media

Front 73

What is the treatment for Bronchiolitis?

Back 73

1. Humidifying O2
2. ABG's
3. Bronchodilators
4. Goggles for healthcare workers --> RSV (contacts are not sufficient)

Front 74

What is atelectasis?

Back 74

A collapsed lung

Front 75

What is the pathology of Epiglottitis?

Back 75

- Microorganism (virus or bacteria) localizes in supraglottic area causing rapid and potentially fatal infection which can lead to cellulitis
- Causes rapidly progressing cellulitis of the epiglottis

Front 76

What are the 6 clinical manifestations of Epiglottitis?

Back 76

1. Drooling
2. Dysphagia
3. Dysphonia: difficulty speaking
4. Inspiratory stidor on the inspiration
5. Retractions
6. Oropharynx is edematous and "cherry red"

Front 77

What is the 2 treatments of Epiglottitis?

Back 77

- A medical emergency (due to cherry red and closing)
- ABX
- Possible intubation

Front 78

What is the pathogenesis of Croup?

Back 78

- An infectious agent causes inflammations in the entire airway with edema formation in subglottic area
- An acute viral inflammation of the larynx
- Affects children 6 mos. to 3 yrs.

Front 79

What are the clinical manifestations of croup?

Back 79

-Barking cough (clue) with stridor

Front 80

What are the treatments for croup?

Back 80

- Outpatient: Mist, oral hydration, avoid stimulation
- Child should being to improve in days
- Inpatient: O2, Pulse Ox., Nebulizer with Epinephrine to help with antigen/ AB reaction, poss. intubation

Front 81

What are the four types of treatments for Lower respiratory disorders?

Back 81

1. ABX: with the presence of the infection
- Broad spec first, change when known which bacteria is present
2. Metered Dose Inhalers:
- Bronchodilators: Beta agonist and anticholinergic
- Anti inflammatory inhalers: corticoseroids
- Last drug: Leukotriene Antagonists
3. O2
4. Oral Corticosteroids

Front 82

What are the uses for Bronchodilator drugs and why are they used?

Back 82

- Used when bronchioles constrict because of the massive inflammatory response --> secretions and edemitis
1. Used to treat chronic pulmonary diseases
2a. Asthma
2b. Chronic Bronchitis: In the bronchioles (only work where there are muscles --> not in the alveoli)
2c. Emphysema

Front 83

What are the 9 side effects of Beta Agonists?

Back 83

1. Tachycardia
2. Tremor
3. Angina (most common)
4. Possible chest pain
5. Nausea
6. Increased anxiety with sweating --> decreases
7. Headaches
8. Dizzyness
9. Metallic taste in mouth

Front 84

What are the 8 nursing implications of Beta Agonists?

Back 84

1. Assess for knowledgsed e deficit
2. Assess for proper administration and effectiveness
3. Know when effective teaching is appropriate
4. Assess for need to switch from MDI to nebulizer
5. Assess for previous intolerance to other sympathetic agents
6. Diabetics w/ high blood sugar --> corticosteroids --> hyperglycemia
7. Elderly sensitive to dose, may need adjustments
8. Rinse mouth after every use due to possible systemic side effects

Front 85

How are beta agonists administered and what should be noted?

Back 85

- Administered via. MDI with spacer
- Typical dose is 2 puffs 1 minute between each
- 1st starts bronchodilation
- 2nd increases the effectiveness
- Calculate the length of time the inhaler will last
- Instruct to monitor decrease in effectiveness not to increase without consulting a physician

Front 86

What are the characteristics of a short acting Beta agonist?

Back 86

- Short acting --> effective
- Albuterol is the most common, rescue drug
- Stimulates beta 2 receptors to achieve dilation - Stimulates ciliary motility --> increases secretion movement out
- Inhibits release of some histamine --> CES
- Administration: inhaled onset 5-15 min, peak is 1-1.5 hrs., duration is 3-6 hours
- Repeated after 15 min if needed

Front 87

What is a Metered Dose Inhaler (MDI)?

Back 87

- Intolerance to beta 2 effect develops over time.
- Used with a spacer to deliver the mediation more effectively
- more portable than a neutralizer and works quicker

Front 88

What is a Nebulizer?

Back 88

- Deliver the drug slowly over several minutes, bronchi gradually dilate and the drug gains deeper access to the lungs
- Used for people with Osteoarthritis and upper extremity weakness or tremors

Front 89

What are the characteristics of a long acting beta 2 agonist?

Back 89

- Keeps the Beta 2 open longer
- Onset 20 min., Peak 3-4 hrs, Duration 12 hrs
- Twice day dosing 12 hrs apart
- not to be used for children under 12 due to tachycardia and anxiety
- Has the same side and nursing management effects as short acting

Front 90

What is the #1 short acting beta 2 agonist?

Back 90

Albuterol

Front 91

What is the #1 long acting beta 2 agonist?

Back 91

Serevent (not a rescue drug)

Front 92

Which anticholinergic drug is combined with albuterol?

Back 92

Combivent

Front 93

What is the #1 anticholinergic bronchodilator?

Back 93

Atrovent: an atropine derivative

Front 94

What is the normal dose and management of Anticholinergic bronchodilators?

Back 94

- Not a rescue drug, do not mix with cromolyn
- Onset 5-15 min, peak 1-2 hrs, duration 3-6 hours
- MDI or nebulizer administration

Front 95

What are the 5 side effects of Anticholinergic bronchodilators?

Back 95

1. Dry mouth
2. Headache
3. Stomatitis (due to dry tongue): important to keep the tongue moist
4. May exacerbate urinary retention
5. May exacerbate glaucoma

Front 96

What is the #1 Methylxanthine bronchodilator?

Back 96

- Theophylline: given by IV must be watched (very dangerous)

Front 97

What are the characteristics of Methyxanthine therapy?

Back 97

- Great broncho dilator (very effective)
- Works by inhibiting the enzyme phosphodieterase or blocking the receptor of adenosine
- Has a narrow therapeutic index
- Effectiveness and 1/2 life varies by age, disease process, and drugs
- Used in ER and intensive care units
- Given orally or IV

Front 98

What are the nursing management for Methyxanthine therapy?

Back 98

1. Monitor for toxicity: check MD orders or facility for norms on drug levels --> look for plasma levels
2. Early s/sx of poss toxicity: nausea, anorexia, hyperirritability, insomnia
o Nausea and anorexia are not common sym. Of respiratory disorders (clues)
3. Toxic s/s: seizures and lethal arrhythmias
4. Instruct to take the drug at the same time every day.
5. Instruct about dietary effects:
o High protein low CHO diet – increases elimination --> what we want
o Low protein high CHO diet – decreases elimination
o Charcoal broiled foods – increases elimination
6. Avoid caffeine use in all forms
7. Drink at least 8 glasses of water a day (peds will use maintenance levels)
8. Cigarette smoking will decrease ½ life by 50%: increase the dose
9. Drugs that increase (fluoroquinolones availability) or decrease (phenobarbital, Dilantin, rifampin) levels

Front 99

What are the characteristics of Anti-inflammatory agents?

Back 99

1. Most Common: Inhaled Glucocorticoids --> Steroids
2. First line agent in prophylaxis of chronic asthma --> inhaler for bronchoconstriction and inhaler for stabilization of the cells
o Asthma --> Trigger --> Mast cells degranulation --> produce histamine --> CES --> stay intact/ rebound
3. A suppressive therapy:  suppresses the inflammatory response
o Decreases synthesis and release of inflammatory mediators
o Decreased infiltration and activity of inflammatory cells
o Decreased edema of the airway mucosa
o Increase in number of beta 2 receptors thus increasing responsiveness to agonist therapy
- If it stops inflammation it will stabilize the inflammatory membranes and make them more receptible

Front 100

What are the inflammatory mediators?

Back 100

COX and leukotriene’s

Front 101

What are some inflammatory cells?

Back 101

Mast cells

Front 102

How will anti-inflammatory agents stabilize the airway mucosa?

Back 102

Inhibit COX to be released --> prostaglandins --> Inflammation 4 --> Decrease edema of the airway --> decrease COX --> decrease 4 inflammatory responses

Front 103

What are the characteristics of Inhaled steroids (glucocorticoids)?

Back 103

1. Always administer 15 minutes after use of beta 2 agonist – Not a rescue drug
1a. Used with albuterol --> the only rescue drug
2. Specificity decreases toxic side effects
3. Common SE are oral candidiasis and dysphonia:
o Treat by rinsing and gargling after each use
o Use of a spacer
4. Stunted growth is seen in children:
o Monitor height and growth (monitor by use of standard charts) --> due to chronic use
5. Long term chronic use will suppress adrenal function --> anytime we have a pt on steroids we will pull them off gradually --> taking a pt off suddenly will cause the adrenal function to have a massive stress response --> tachycardia
o Monitor for reduce responses to stress --> the stress of disease (physical stress)

Front 104

What are the four common inhaled glucocorticids?

Back 104

1. Beclomethasone – Beclovent
2. Fluticasone – Flovent, Flonase --> allergic rhinnitus
3. Triamcinoclone – Azmacort
4. Flunisolide – Aerobid

Front 105

What are the characteristics of oral steroids?

Back 105

- Try to avoid using on a chronic basis
- Alternate dosing is recommended if needed on a long term basis

Front 106

What are the 5 common complications of oral steroids?

Back 106

1. Hyperglycemia – both long and short term
2. Osteoporosis
3. Adrenal suppression
4. Stunted growth --> Pediatric
5. Peptic ulcer disease

Front 107

What are the three openings in the duodenum?

Back 107

1. Aorta
2. Vena Cava
3. Esophagus

Front 108

What are the three upper sections of the airway?

Back 108

1. Nasopharynx
2. Oropharynx
3. Laryngopharynx (Larynx)

Front 109

What are the six sections of the lower airway?

Back 109

1. Trachea
2. Bronchi
3. Carina
4. Bronchioes
5. Alveolar ducts
6. Alveoli

Front 110

How thick is the alveoli?

Back 110

-1 cell think; very thin and fragile

Front 111

What is surfactant?

Back 111

- A surface tension reducing agent produced by type II pneumocytes in the lung
- Facilitates gas exchange and lowers surface tension

Front 112

What are the 3 types of cells in the alveoli?

Back 112

1. Epithelial Structure Cells
2. Produce Surfactant
3. Alveolar Macrophages- Phagocytes

Front 113

What is the capillary network and how much can it expand?

Back 113

- Network for exchange of O2 and CO2
- A low pressure system that can expand 2-3x before significant pressure changes occur. ie. sex or exercise

Front 114

What is fluid balance?

Back 114

- Alveolar edema is more serious than interstitial edema because if the alveoli become edemitis we will not have gas exchange

Front 115

What is capillary edema and its three parts?

Back 115

1. Edema -->
2. Recruitment (opening previously closed alveoli) -->
3. Distention (widening of capillary vessels)

Front 116

What is the difference between Chemoreceptors and Baroreceptors?

Back 116

- Chemoreceptors are chemical receptors O2 and CO2
- Baroreceptors are pressure that effects respiration when B/P changes

Front 117

What should always be checked first when a person is unconscious or their CNS is interrupted?

Back 117

1. Airway
2. Breaths
3. Circulation

Front 118

What is hypoxia and how does it relate to hypoxemia?

Back 118

Hypoxemia: a lack of O2 in the blood leads to Hypoxia: a lack of O2 in the body

Front 119

What are the four Bronchodilators and their medications?

Back 119

1. Long acting Beta 2 agonist: Serevent
2. Short acting Beta 2 agonist: Albuterol
3. Anticholinergic: Atrovan
4. Methylzanthines: Theophylline

Front 120

What are the medications and classifications that use MDIs?

Back 120

1. Bronchodilators
1a. Beta 2 Agonist (long: Serevent and short: Albuterol)
1b. Anticholinergic (Antrovent)
2. Anti-Inflammatorys
2a. Glucocortcoids
1. Beclovent
2. Flovent, Flonase (allergic rhinnitus)
3. Azmacort
4. Aerobid

Front 121

What are the two types of Allergic Rhinitis?

Back 121

1. Seasonal (hay fever)
2. Perennial (indoor)

Front 122

What are the 3 affected areas of allergic rhinitis?

Back 122

1. Upper airway
2. Lowe airway
3. Eyes --> a secondary presentation

Front 123

What are the three types of drugs used for allergic rhinitis and how are they administered?

Back 123

1. Glucocorticoids (Intranasal)
2. Antihistamine (oral and intranasal)
3. Sympthomimetic (oral and intranasal)

Front 124

What are the 4 mechanisms of action for Glucocorticoids?

Back 124

1. Congestion
2. Rhinorrhea
3. Itching
4. Sneezing
- Blocks mast cell degradation

Front 125

What are the 3 mechanisms of action for Antihistamine?

Back 125

1. Rhinorrhea
2. Itching
3. Sneezing
- Blocks mast cell degradation

Front 126

What is the 1 mechanism of action for Sympathomimetic?

Back 126

1. Congestion

Front 127

What are the 3 requirements for simple diffusion?

Back 127

1. Intact non-thickened alveolar walls
2. Intact non thickened capillary walls
3. Minimal interstitial space w/o additional fluid

Front 128

Where does simple diffusion occur?

Back 128

- In the pulmonary calculation at the pulmonary capillary bed

Front 129

How many liters of air are filtered, warmed, and humidified?

Back 129

- Approx. 10,000 liters

Front 130

How many RBC are there normally

Back 130

4.8-5.4 million

Front 131

How many Leukocytes are there normally?

Back 131

5,000-9,000

Front 132

How many WBC are indicative of an infection?

Back 132

more than 9,000

Front 133

What is the normal number of platelets?

Back 133

300,000

Front 134

When is there an abnormal amount of platelets?

Back 134

below 150,000

Front 135

At what number of platelets can you see Petechae (bleeding in the skin)?

Back 135

100,000

Front 136

At what number of platelets is there spontanious bleeding?

Back 136

20,000

Front 137

What is the normal range of hematocrit for men?

Back 137

40-50% or 45%

Front 138

What is the normal amount of hemoglobin for men?

Back 138

13.8-18 grams per deciliter

Front 139

How does ARDS develop and what is the mortality rate?

Back 139

- Develops from direct or indirect lung injuries
- Sepsis
- Damage to the alveolar capillary membrane: it becomes more permeable to intravascular fluid --> causing shock

Front 140

What is sepsis?

Back 140

- An infection in the system gets into the blood stream which is then taken throughout the body

Front 141

What are the 4 results of the alveoli filling up with fluid?

Back 141

1. Severe dyspnea
2. Hypoxia
3. Decreased Lung Compliance
4. Diffuse pulmonary infiltrates

Front 142

What are the 4 changes in the lungs due to ARDS and what causes the changes?

Back 142

- Changes caused by Neutophils being attracted and releasing mediators
1. Increased pulmonary capillary membrane permeability (leaking capillaries)
2. Destruction of Elastin and Collagen
3. Formation of pulmonary micoroembli
4. Pulmonary artery vasoconstriction

Front 143

Where is the interstitium and what happens when it fills with fluid?

Back 143

- The area between the pulmonary capillary and the alveolus
- When it fills, it becomes difficult for the capillary or the alveoli to expand

Front 144

What are the 5 Clinical Manifestations of ARDS?

Back 144

1. Increase work of breathing
2. Increase Respiratory Rate
3. Decreased tidal volume
4. Decrease in surfactant
5. Interstitial, alveolar, and interstitium edema

Front 145

What are the 3 functional/histological changes in ARDS?

Back 145

1. Atelectasis resulting in V/Q mismatch
2. Shunting of the pulmonary capillary bed
3. Hypoxemia unresponsive to increasing concentrations of O2

Front 146

What are the 7 manifestations that occur 1-2 weeks after an initial lung injury in ARDS?

Back 146

1. Influx of neutrophils, monocytes, and lymphocytes
2. Fibroblast proliferation
3. Lung becomes dense and fibrous
4. Lung compliance continues to decrease
5. Hypoxemia worsens due to thickened alveolar membrane (worst problem)
6. If reparative phase persists, widespread fibrosis results
7. If phase is arrested, lesions resolve

Front 147

What are the 2 manifestations that occur 2-3 weeks after the initial lung injury in ARDS?

Back 147

1. Lung is completely remodeled by sparsely collagenous and fibrous tissues (everything gets hard)
1a. Decreased lung compliance
1b. Decreased area for gas exchange
2. Pulmonary Hypertension resulting from vascular destruction and fibrosis

Front 148

What are the 7 early clinical manifestations of ARDS?

Back 148

1. Dyspnea
2. Tachypnea
3. Cough and scattered crackles
4. Restlessness (LOC)
5. CNS mediated: high Poxemia
6. ABG's: Mild hypoxemia and respiratory alkalosis caused by hyperventilation
7. Chest X-ray: many show scattered interstitial infultrates in the interstitium

Front 149

What are the 9 late clinical manifestations of ARDS and why do symptoms worsen?

Back 149

- Symptoms worsen due to fluid accumulation, decreased lung compliance and lung volume
1. Whiteout or white lung seen in x-ray
2. Tachycardia
3. Cyanosis
4. Pallor
5. Diaphoresis (sweating)
6. Changes in sensorium (decreased consciousness)
7. Decreased mentation (mental activity, thinking)
8. Substernal Retractions
9. Hyoxemia and a PaO2/FIO2 ratio <200 despite increased FIO2 (supplemental O2)

Front 150

What causes a whiteout or white lung?

Back 150

- Due to consolidation and widespread infiltrates throughout the lung

Front 151

What are the 5 treatments for ARDS?

Back 151

1. Endotracheal Intubation
2. ID the underlying cause
3. Fluid Resuscitation F&E checks
4. Ventilator Support
4a. PEEP: positive end-expiratory pressure
5. Block the inflammatory response

Front 152

What does IRDS stand for and what is it's other name?

Back 152

- Infant respiratory distress syndrome
- Also referred to as Hyaline Membrane Disease

Front 153

When does surfactant begin to be produced and how long does it take for it to be in the alveoli?

Back 153

- Produced at 27 weeks
- Needs 4 weeks to be placed in all the alveoli

Front 154

What causes IRDS?

Back 154

- Surfactant deficiency: increases in alveolar surface tension and decreases compliance 1/5-1/10 of normal

Front 155

What causes acidosis?

Back 155

- Shallow breaths that do not expel CO2: hyperventilation

Front 156

What causes alkalosis?

Back 156

- Expelling CO2 through deep breaths

Front 157

What is the difference between ARDS and IRDS?

Back 157

- Similar features in both
- In IRDS there is not have a functional lung

Front 158

What are the 6 clinical manifestations of IRDS at birth?

Back 158

1. Dyspnea
2. Tachypnea
3. Retractions: all three
4. Flaring of nares
5. Hypotension
6. Low temperature: due to the brain needing O2
= all the signs of shock

Front 159

What are the 8 treatments for IRDS?

Back 159

1. Ventilation
2. Incubate and ventilation support
3. High Frequency Jet Ventilation
4. Exogenous Surfactant
5. Fluid resuscitation F&E checks
6. Block the inflammatory response
7. ABX
8. Thermoregulation

Front 160

What characterizes a primary pnemothorax?

Back 160

- A spontaneous pneumothorax primarily in tall thin men 20-40 and increased risk due to smoking

Front 161

What is a Pneumothorax?

Back 161

- An accumulation of air in the pleural space

Front 162

What characterizes a secondary Pneumothorax?

Back 162

- Results from complications form pre-existing pulmonary disease ie. Asthma, Emphysema, Cystic fibrosis, infections (pneumonia or TB)
- Underlying cause is from an abscess that bleeds

Front 163

What characterizes a third Pneumothorax?

Back 163

- Tension Pneumothorax: pressure causing a mediastinal shift (away from the midline)

Front 164

What are the two types of a third Pneumothorax?

Back 164

1. Hemothorax: Accumulation of blood
2. Chylothorax: Accumulation of lymph

Front 165

When there is an Acaletasis, what will be heard, what is it, and what happens to the great vessels?

Back 165

Dextrocharia: When the heart has turned on itself
- Great vessels will twist and turn
- The systemic system will be compromised and cut off from O2 and neutrients

Front 166

What are the clinical manifestations of a Pneumothorax?

Back 166

VS: Tachycardia, dyspnea, hypotension decreased breath sounds on affected side
Pain: Sudden and sharp on affected side
Neck: Jugular vein distrophy, tracheal shift (indicative of the heart starting to turn)

Front 167

What are the 2 differences between ARDS and a Pneumothorax?

Back 167

1. Pneumothorax has decreased breath sounds on the affected side
2. Pneumothorax has sudden sharp pain the the affected side

Front 168

What is the treatment for a Pneumothorax?

Back 168

- Treatment is symptomatic
- Chest tube at the 4th intercostal arterial axillary

Front 169

Why would there be a low placed chest tube?

Why would there be a high placed chest tube?

Back 169

Low: For draining out the hydrothorax and pneumothorax

High: for draining the pneumothorax

Front 170

What is the size of the needle decompression and where is it inserted?

Back 170

- 14 or 16 gage needle ar the 2nd or 3rd intercostal midclavicular

Front 171

What are the 3 components of the Chest tube?

Back 171

1. Suction system: tube from the pt to the wall
2. Underwater seal bottle
3. Collection chamber: important to monitor fluid level

Front 172

What are the 3 nursing requirements while monitoring a chest tube?

Back 172

- Monitor:
1. All all vital sounds and chest sounds
2. Chest tube function
3. Resolution of the underlying pathology

Front 173

What are the 3 etiologies of pneumonia?

Back 173

- Can be bacterial, fungal, or viral
1. Aspiration of normal bacterial flora
2. Inhalation of contaminants
3. Contamination from the systemic circulation

Front 174

What are the 3 classifications of pneumonia?

Back 174

1. Community acquired (bacterial)
2. Hospital acquired: must make sure settings and O2 are right
3. Ventilator associated pneumonia

Front 175

What are the clinical manifestations of pneumonia and what determines them?

Back 175

- Determined by the pathogen
Bacterial: Chills, cough, purulent sputum, abnormal chest radiograph
Viral: Upper respiratory prodrome (fever, coryza, course hoarseness) accompanied by wheezing and or rales, productive cough
- No fever is indicative of chlamydia

Front 176

What is the treatment for pneumonia?

Back 176

- Match the bug to the drug
- ABX

Front 177

What is the narrow spectrum ABX for Pneumonia?

What is the broad spectrum ABX for Pneumonia?

Back 177

Narrow: Pen G

Broad: Ampicillin and Amoxicillin

Front 178

How is Pneumonia diagnosed?

Back 178

- Chest x-ray: identify an isolated area
- High WBC indicative of infection

Front 179

Are the venuels, arterials, and lymph vessels affected by the inflammation response?

Back 179

Yes, because they are all hit with the pressure from the edema

Front 180

Is the fluid of fungus different from fluid from a virus?

Back 180

Yes, fungus fluid is thinker and more difficult to expel