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NURS 316 > Quiz 2 > Flashcards

Quiz 2 Flashcards

1
Q

Nasal Cavity and the Mouth

A

Air is inhaled and enters the body through the mouth and nasal cavity
- Warmed up through the process

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2
Q

Parts of the Respiratory System

A

Conducting Airways:
- Through which the air moves between the lungs and atmosphere
(nasal passages, mouth, nasopharynx, larynx and tracheobronchial)

Respiratory Airways:
- Lungs are the functional structures of the res system
- Lobules are the smallest functional unit of the lungs, consisting of the res bronchioles, alveoli and pulmonary Caps, responsible for gas exchange

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3
Q

Trachea Function

A
  • Air passes down the trachea
  • Trachea is a long tube connecting the mouth and nasal cavity of the rest of the Res system
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4
Q

Bronchus Function

A
  • Trachea branches off into two bronchi
  • One bronchus enters each lung
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5
Q

Bronchioles

A
  • Each bronchus divides into smaller tubes called bronchioles which the air passes through
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6
Q

Alveoli

A
  • Alveoli are located at the end of each bronchiole
  • Alveoli are air sacs which facilitate gas exchange
  • There are millions of them in the lungs
  • Alveolar macrophages are responsible for the removal of offending particles from the alveoli
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7
Q

Alveoli Features

A
  • Thin walls to reduce the distance for diffusion
  • Walls are only one cell thick
  • Have a large surface area which is moist so gases can dissolve and diffuse across
  • Surrounded by caps, so alveoli have a rich blood supply
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8
Q

Gas Exchange

A
  • Inhaled O2 diffuses from the alveoli into the blood
  • Inhaled Nitrogen cannot diffuse so it doesn’t enter the blood stream
  • CO2 diffuses from the blood into the alveoli to be exhaled
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9
Q

Pleura

A
  • Double-layered membrane that surrounds each lung
    2 Parts:
  • VISCERAL = adheres to the lung surface
  • PARIETAL = lines chest wall
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10
Q

Pleural Cavity

A

Thin space between both pleura

  • Thin film of serous fluid that reduces friction during respiration
  • Potential space for excess fluid or inflammatory exudates to accumulate
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11
Q

Ventilation

A

Movement of gasses in and out of lungs

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12
Q

Inspiration

A

Chest cavity EXPANDS

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13
Q

Expiration

A

Chest cavity becomes SMALLER

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14
Q

Lung Tissue Composition

A

1) Elastin
2) Collagen
When elastin fibres are replaced by scar tissue, the lungs become stiff and non-compliant (not as stretchy as before)
Pulmonary Congestion and edema also result in a reversible decrease in pulmonary compliance

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15
Q

Pulmonary Compliance

A

Extent to which lungs expand

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16
Q

Pulmonary Function Tests

A

Spirometry = physiological test that measures the ability to inhale and exhale air relative to time
- Diagnostic test of several common respiratory diseases
- Test for FVC, FEV-1.0, % of FVC)

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17
Q

Forced Vital Capacity (FVC)

A

Max amount of air that can be rapidly and forcefully exhaled from the lungs after full inspiration

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18
Q

Forced Expiratory Volume in 1 second (FEV-1.0)

A

Volume of air expired in the first second of FVC

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19
Q

% of FVC

A

Volume of air expired in the first second, expressed as a percentage of FVC

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20
Q

Lung Perfusion

A
  • Flow of blood through blood vessels in the lungs
  • Essential for the exchange of O2 and CO2
  • Blood flows through the lungs, it picks up O2 from the air we breathe and releases CO2 to be exhaled
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21
Q

Ventilation-Perfusion Ration (V/Q)

A
  • Compares the amount of air that gets into the lungs (ventilation) to the amount of blood flowing through the lungs (perfusion) to assess how well the lungs are bringing in O2 and getting rid of CO2 (should be almost even = 1.0)
  • Healthy lungs = V/Q ratio is typically around 0.8 (slightly more blood flow than air reaching the alveoli)
  • Conditions like PNEUMONIA make it hard for air to get in and BLOOD CLOTS (PULMONARY EMBOLISM) in the lung can block blood flow affect V/Q ratio and overall lung function
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22
Q

What Affects Gas Diffusion?

A
  • Characteristics of gas (eg CO2 diffuses 20x faster than O2)
  • Concentration of gas (differences in partial pressure on either side of the membrane)
  • Thickness of alveolar-capillary membrane
  • Surface area of lung tissue (diseases destroy lung reduce surface area and diffusion)
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23
Q

Arterial Blood Gases

A
  • Blood gas measurement are used to determine the partial pressure of O2 (PO2) and CO2 (PCO2)
  • Arterial blood is preferred for measuring blood gases because venous levels of O2 and CO2 reflect the metabolic demands of the tissues rather than the gas exchange function of the lungs
    NOT AS IMPORTANT TO KNOW NOW (WILL LEARN MORE NEXT SEMESTER)

Normal Values:
pH = 7.35-7.45
PaO2 = 80-100mmHg
PaCO2 = 35-45mmHg
HCO3 = 22-26mmol/L
BE = -2 - +2
SaO2 = 94-100%

Respiratory Acidosis
Respiratory Alkalosis (CO2 is lower)

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24
Q

Innervation

A

Lungs innervate by the sympathetic and parasympathetic divisions of the autonomic NS

**PARASYMP NS:
(Cholinergic receptors)
- Stimulation leads to bronchial constriction and increased glandular secretions

**SYMP NS:
- B2 Adrenergic receptors
- Stimulations cause airway relaxation, blood vessel constriction and inhibition of glandular secretion

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25
Q

Lung Diseases

A

Restrictive Lung Disease
Obstructive Lung Disease
Airway Disease
Lung Tissue Disease
Lung Circulation Disease

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26
Q

Restrictive Lung Disease

A

Lung tissue or chest muscles can’t expand enough
- Creates problem with air flow because less lung volume
Eg) Pulmonary Fibrosis

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27
Q

Obstructive Lung Disease

A

Air has trouble flowing out of the lungs because of airway resistance
= slower flow of air
Eg) Asthma, chronic bronchitis, emphysema, COPD

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28
Q

Asthma Defintion

A

Chronic inflammatory disorder of the airways (NOT autoimmune) that causes episodes of airway obstruction, bronchial hyper-responsiveness, airway inflammation and sometimes airway remodelling
- Muscles tighten, airways swell, Mucus clogs the airways, lungs have difficulty moving in and out
- Inflammation + pro-inflammatory mediators activating further inflammation
- Mast cell degranulation
- MORE BREATHING ISSUE THAN MUCUS ISSUE (COPD is more Mucus)

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29
Q

Asthma Clinical Presentation + Asthma Attacks

A

Epithelial injury in the bronchi = chronic hypersensitivity ‘reactivity’ of the bronchial airways
- Risk of Attacks = exposure triggers acute ‘attacks’

Asthma Attack S&S:
- Wheezing, shortness of breath, reduced air entry into lung lobes, chest tightness, tachy, anxiety, panic, fatigue
- Inability to speak in full sentences (classic sign of shortness of breath)
- Limited inspiration + longer expiration phase = air trapping in alveoli
- hyper-inflated lungs w/ limited gas exchange
- V/Q mismatch
- Low O2 & High CO2
- Hypoxemia, hypercarbia & high pulmonary pressures

30
Q

Asthma Treatments

A

Drugs used to stabilize asthma = MAINTENANCE drugs

Drugs used during asthma attack = RESCUE drugs

31
Q

Management of Asthma

A
  • Stabilizing the bronchial inflammation & minimizing the number of attacks
  • Avoidance of triggers
  • Acquire control of the inflammation with a daily treatment protocol & compliance
  • Proper use of inhaler, proper dose, avoidance of respiratory infections
32
Q

Maintenance TX of Asthma

A

Inhaled anti-inflammatory drugs exert local effect in bronchioles causing low systemic = low side effects
Administered Daily to control triggers

GLUCOCORTICOIDS:
- 1st line for maintenance/prophylaxis treatment against asthma attacks
- Drugs = Budesonide (Pulmicort), Fluticasone (Flovent), Beclomethasone (Qvar)
- Administration = Inhalers, nebulizers

MAST CELL STABILIZERS:
- Inhibit histamine release from mast cells
- Drug = CROMOLYN: Inhaler, slow onset of therapeutic level, frequent dosing (3-4x/day), not common as 1st choice, synergy w/ glucocorticoids

LEUKOTRIENE MODIFIERS:
- Block leukotriene receptors
- Modify inflammatory response “pre-exposure (prophylaxis)
- Drugs = MONTELUKAST (singulair): Administered PO, Systemic effects, slow onset of action, synergy treatment

BIOLOGICS: MONOCLONAL ANTIBODIES
Drug = OMALIZUMAB (XOLAIR)
- Binds free IgE = Decreased antigen binding = no degranulation, decreases expression of mast cell-bound IgE = no degranulation
Long term treatment plan

33
Q

What does SNS stimulation cause in Asthma Treatment?

A

B Agonist = SUPPORTS Sympathetic, bronchiodilator

Cholinergic Antagonist (anticholinergic) = ANTAGONIZE parasympathetic, Bronchodilation

34
Q

Acute Tx of Asthma (Rescue)

A

Treat Bronchioconstriction via Inhaler or Nebulizer

BETA-2 ADRENERGIC AGONIST:
- Stimulates sympathetic NS B2 receptors directly
Drugs = Salbutamol/Albuterol (Ventolin)
Formoterol

ANTICHOLINERGICS:
- Antagonize Parasympathetic NS, causing bronchodilation
- Less potent & has slower onset of action
- Synergic w/ Beta-2-Agonists
Drugs = Atrovent (Ipratopium)

35
Q

STATUS ASTHMATICUS

A

Severe asthma Attack (ER Admission)

S&S = Severe SOB, Assessory muscle use, cyanosis, chest tightness, anxiety/panic

Treatment:
- O2 Therapy
- Beta-Adrenergic Agonist (ventolin via NEBULIZER
- Magnesium Sulfate
- Glucocorticoids (Dex)
- Anticholinergics via NEBULIZER
- Sympathomimetrics = Epinephrine IV (potent w/ short half life, goal is bronchodilation, side effect - SNS Stimulation)

36
Q

Magnesium Sulfate

A

NO is a potent vasodilator***
Electrolyte, calcium channel blocker
Can be titrated to alleviate severe bronchoconstriction

37
Q

Asthma VS Anaphylaxis

A

Asthma:
- CHRONIC
- Triggers = Allergens (Eg pollen, dust mites), irritants (smoke), exercise, respiratory
- Symptoms = Wheezing, coughing, SOB, Chest Tightness, Episodic & vary in severity

Anaphylaxis:
- SUDDEN ONSET = Severe, life-threatening allergic reaction that can occur
- Triggers = foods, insect stings, medications or latex
- Symptoms = Rapid onset of difficulty breathing, swelling of the throat, hives, low BP, GI symptoms

SIMILARITIES:
- Both treated w/ epinephrine when unsure
- Cyanosis

38
Q

Chronic Obstructive Pulmonary Disease (COPD)

A

Chronic Bronchitis + Emphysema

Risk Factors:
- Smoking (main cause)
- Long term exposure environmental pollutants and chemicals
- >40 yrs old

39
Q

Chronic Bronchitis

A

Irreversible damage to bronchial tubes to persistent inflammation and irritation of the airway tubes that causes narrowing/obstruction
- Causes SOB, cough, and excess mucus production
Symptoms = Long-term cough with sputum
Progressive disease**

40
Q

Emphysema

A

Permanent damage and loss of elasticity in alveoli, leading to poor recoil and air trapping (poor exhalation = increased CO2)
SYMPTOMS = pursed-lip breathing, tripoding, barrel chest

41
Q

Management of COPD

A
  • Smoking Cessation = MOST EFFECTIVE step in managing COPD
  • O2 Therapy (caution CO2 Retention*** 88-92% SPO2 for COPD patients)
  • Vaccinations (influenza and pneumonia vaccinations to prevent infections that might exaacerbate COPD

MEDICATIONS:

Bronchodilators - Beta-Agonists (Albuterol = short-acting, Formoterol = Long-acting), Anticholinergics

Inhaled Corticosteroids - Budesonide, flutincasone

Combination Inhalers -
Advair = Salmeterol (LABA) + Fluticasone (Advair) (What Jovan takes)

Mucolytics -
Acetylcysteine in nebulizer to loosen sputum

42
Q

Nursing Considerations R/T COPD

A

Assessment:
- Res Status (Monitor res rate, effort, & lung sounds. Assess for hypoxia and hypercapnia)
- O2 Sats

Medication Management:
- Administer meds and education patient on the proper use of inhalers, nebulizers and any combination medications to ensure effective delivery meds
- O2 administration as needed (educate on fire hazards if leaving w/ O2)

Patient Education:
- Educate pt about COPD, its progression, and self management (recognizing early signs of exacerbations like increased breathlessness, changes in sputum colour and volume)
- Provide information on the risks of smoking and support for cessation including referral to smoking cessation programs

Breathing Techniques:
- Pursed-lip-breathing = reduce dyspnea and improve ventilation

Energy Conservation:
- Educate patients on techniques to conserve energy during daily activities

Nutrition:
- Monitor nutritional status and provide education on a balanced diet (small meals high in protein and calories to maintain strength)

Hydration:
- Lots of water to help thin mucus secretions

Psychosocial Support:
- Provide support and referrals to mental health services and support groups as needed

43
Q

Acute Inflammation

A
  • The body’s early protective response to an injurious agent
  • Primary function is to CONTAIN INJURY, STIMULATE IMMUNE RESPONSE, REMOVE DEBRIS, PROTECTING THE BODY AGAINST INFECTION AND PROMOTING HEALING

Signs: redness, swelling, heat, pain and loss of function

44
Q

2 Phases of Acute Inflammation

A

VASCULAR PHASE:
- Affects small blood vessels at the side of injury
- Starts w/ Momentary vasoconstriction
- Then Vasodilation increases caps blood flow (causing heat and redness)
- Then Vascular Permeability

CELLULAR PHASE:
- Involves the delivery of leukocytes (mainly neutrophils) to the site of injury for phagocytosis
- Involves endothelial activation, adhesion and margination, transmigration and chemotaxis
- After extravasation, leukocytes migrate towards site of injury by chemotaxis

45
Q

Vascular Permeability

A

Leakage of fluid (exudate) from blood vessels into extracellular space, causing swelling (edema), pain and impaired function
- Exudate also contains CLOTTING FACTORS to prevent the spread of infectious agents throughout the body

46
Q

Acute Phase Response

A

Systemic Manifestation of Inflammation
- Mediated by the release of Cytokines
- Stimulates liver to produce acute-phase proteins
- Communicates with the hypothalamus to produce fever
- Stimulates leukocytes in the bone marrow
- Facilitate metabolic changes such as the breakdown of protein into amino acids that can be used by immune system or for tissue repair

47
Q

Systemic Inflammation Response Syndrome (SIRS)

A
  • Large amounts of microorganism in the blood = disregulation of inflammatory response = large amount of cytokines released
  • Vasodilation increased vascular permeability, intravascular fluid loss, circulatory shock
48
Q

Inflammatory Mediators

A

HISTAMINE
ARACHIDONIC ACID METABOLITES
PLASMA PROTEINS

49
Q

Histamine

A
  • Causes dilation of blood vessels, smooth muscle constriction, tissue swelling and itching
  • PRINCIPAL MEDIATOR of immediate transient phase of increased vascular permeability in acute inflammatory phase
  • Found in tissue and also released by most mast cells
50
Q

Arachidonic Acid Metabolites

A

Prostaglandin:
- Present in most tissues and stored and released by mast cells
- Increases cap permeability, attracts WBC to site of inflammation, causes pain, potentiates effects of histamine and promotes platelet aggregation

Leukotrienes:
- Effects similar to histamine but more potent
- Also causes slow and sustained bronchiocontriction

51
Q

Plasma Proteins

A

CLOTTING:
- Aids coagulation in vascular phase

COMPLEMENT SYSTEM:
Increase vascular permeability improves phagocytosis and causes vasodilation

BRADYKININ:
- increases vascular permeability and causes contraction of smooth muscles

52
Q

Glucocorticoids

A

Systematic steroids are synthetic derivatives of the natural steroid, cortisol produced by adrenal glands
Eg. prednisone, hydrocortisone, Dex

Local Route = joint injections, ear drops, topical creams

Systemic Route = ONLY USED IN ACUTE TREATMENT, risk of systemic side effects w/: Long term treatment & PO vs IV vs IM

Corticosteroids must be weaned off slowly to avoid withdrawal symptoms
- Negative feedback decreases/stops adrenal glucocorticoid synthesis = no abrupt stoppage of treatment

53
Q

Cushing’s Syndrome

A

Overtreatment w/ systemic glucocorticoids = Esaggerated side effects leading to dysfunction of affected systems

54
Q

4 Types of Exudates

A

Serous Exudate:
- Watery fluid, low in protein content (Eg. blisters)
- Results from plasma entering inflammation site
- Serous is a regular part of healing and small amounts are considered normal

Hemorrhagic Exudate:
- AKA Sanguineous
- Occurs w/ significant tissue injury that damages blood vessels or when there is leakage of RBC from caps

Purulent Exudate:
- Thick yellow, brown, green or grey drainage containing pus (degraded WBC, proteins and tissue debris)
- Staphylococcus induces this
- Indicate an active infectious process
Abscess = localized inflammation containing purulent exudate, surrounded by neutrophils

Fibrinous Exudate:
- Contain large amount of fibrinogen to form a thick and sticky meshwork like fibres of blood clot

55
Q

Primary Intention of Wound Healing

A

Edge to edge healing by approximating wound w/ minimal tissue loss
-Eg) Paper cut, sutured surgical wound
= Minimal scarring

56
Q

Secondary Intention of Wound Healing

A
  • Healing from inside out (no closue)
  • Larger wounds w/ greater loss of tissue and contamination
    Eg) burns, large surface wound
    = Slower healing and scar formation
57
Q

Tissue Regeneration

A

Replaces injured tissue w/ cells of the same type (Parenchymal vs Stromal)
- Labile vs Stable vs Permanent cells

58
Q

Fibrous Tissue Repair

A

Replacement by connective tissue

Generation Granulation Tissue:
- Red, moist connective tissue containing new capillaries (formed by angiogenesis) and proliferating fibroblast

Fibrogenesis:
- Influx of fibroblast to secrete components of ECM such as firbonectin proteoglycan, collagen

Although Scar tissue fills the gap created by tissue death, it does not repair the structure with functioning parenchymal cells

59
Q

Stages of Wound Healing

A

Inflammatory Phase:
- Removes injurious agent and prepares wound for healing
- Hemostasis (formation of clots), vascular phase and migrations of phagocytic WBC to wound site
- Wound onset to Day 4
- After 24hr, Macrophages join in phagocytosis and aid production of growth factors for next phase

Proliferative Phase:
- Fibroblasts secrete collagen, growth factors etc that induce angiogenesis and endothelial cell proliferation to form granulation tissue
- Wound space is filled by granulation tissue which supply oxygen and nutrients and act as scaffolding for new tissue growth
- Day 4 through Week 2-6
- Ep cells at the wound edges proliferate to form new surface layers

Remodelling Phase:
- About 3 weeks post-injury
- Decrease in vascularity and continued remodelling of scar tissue thru simultaneously synthesis of collagen and lysis by collagenase to increase the strength of the scar tissue and shrink the scar to make it less visible

60
Q

Factors that Affect Wound Healing

A

Blood Flow and O2 Delivery
Malnutrition
Age
Impaired Inflammatory and Immune Responses
Infection

COMPLICATIONS:
- Wound Dehiscence = separation of previously approximated wound edges
- Evisceration = Dehiscence w/ protruding organs. Medical Emergency***
(Nursing place saline soaked gauze on the area, lower head of bed and call MD immediately)

61
Q

Chronic Inflammation

A
  • Acute inflammation >10 days
  • May last weeks, months, or even years
  • Causes tissue destruction by repetitive inflammatory cascade
  • Caused by persistent irritants, mostly insoluble or resistant to phagocytosis and other inflammatory mechanisms
  • Agranulocytes typically present, instead of neutrophils
  • Secretion of regenerative mediators Eg) tissue Growth Factors
  • Forming scar Tissue (less vascular, flexible and strong) to replace connective tissue

Repetitive Inflammatory cycle causes cellular tissue changes
- Dysfunction of tissue
- Susceptibility to unusual growth and altered cellular division

62
Q

Allergic Rhinitis

A

Rhinitis = Irritation and inflammation of nasal mucosal, causing nasal congestion, runny nose, sneezing and itching

  • AKA Hay Fever = triggered by inhaled allergens leading to hypersensitivity
  • Seasonal or occasional triggered by pollen, dust, dander etc
  • S&S = rhinitis, conjunctivitis (eyes), headache,
  • Relevant Bloodwork = elevated eosinophils

Treatment:
- Antihistamiens and intranasal corticosteroids for nasal inflammation
- Desensitization

63
Q

Atopic Dermatitis

A

“Eczema”
- Caused by exaggerated IgE/ allergic response
- Chronic inflammation of the skin
- Deficient innate skin barrier, itching scar formation
- Risk of super-infection

Treatment:
- Moisturize, topical glucocorticoids, antihistamines, antibiotics

64
Q

Psoriasis

A

Chronic Inflammatory skin disease
Autoimmune
- Risk Factors = Family history, triggered by skin trauma, climate, stress, medications
- Skin Changes = hyperkeratosis, thinned stratum granulosum, dilated dermal papillae
- S&S = dry, scally skin patches, commonly non-pruritic (not itchy)

Treatment:
- Glucocorticoids, moisturizing cream

65
Q

Eczema Vs Psoriasis

A

E = VERY itchy, Oozing and crusting, appears on flexual skin surfaces

P = NOT very itchy, Scaling, appears on extensor skin surfaces

66
Q

Rheumatoid Arthritis (RA)

A

Chronic systemic rheumatic disease of the joint
- Involves progressive & autoimmune destruction of healthy endogenous tissues
- Risk factors = family history, gender

MOA:
- Inflammation of con tissue, triggered by an immune system attacking joint
- Proliferation of WBC’s and pro-inflammatory mediators within tissue
- Dysfunction of synovial cavity
- Thickening and deformity of affected tissue
- Affects the same joints bilaterally

S&S:
- Swelling, stiffness worse in AM, synovial joint inflammation, soft feeling on joints, symmetrical symptoms, systemic effects (fever, malaise etc)

Relevant Bloodwork = CRP

Treatment:
- No cure**
- Use NSAIDS, Glucocorticoids

67
Q

RA Treatment w/ Immunomodulators

A

Disease Modifying Anti-Rheumatic Drugs (DMARDS):
- Target the underlying immune processes that contribute to inflammation and joint damage, helping to modify the disease course rather than just relive symptoms
- Suppress overall immune system
EG) Methotrexate (FIRST LINE TREATMENT FOR RA**)

Biologics Drugs:
- Subset of DMARDS made up of antibodies derived from living organisms
- Inhibit pro-inflammatory cytokines
Eg) TNF Inhibitors (Infliximab, Adalimumab)

68
Q

Osteoarthritis

A

Degenerative disorder of articular cartilage (“Wear & Tear” arthritis)
- Affects fewer joints than RA
- Risk Factors = mechanical stress, obesity, age, gender (reduced estrogen levels)
- Cartilage changes occur due to…
- Decreased proteoglycans = weakening collagen network = pro-inflammatory mediator release = further inflammation = ongoing inflammation = cartilage tissue destruction = bone-bone in articulating surface

Treatment:
- NSAIDS, glucocorticoids

69
Q

Inflammatory Bowel Disease (IBD)

A

Autoimmune Disease
Eg) Crohn’s & Ulcerative Colitis

Symptoms = diarrhea, fatigue, abdominal pain and cramping, blood in stool, reduced appetite, unintended weight loss
- Attack may be triggered when endogenous GI host flora is recognized as an antigen leading to inflammation

Treatment:
- Aim to treat acute attack and prevent relapse
- Main stay = low dose PO glucocorticoids, DMARDS,
Sulfasalazine

70
Q

Ulcerative Colitis

A

Inflammation, swelling and sores in large intestine (colon) and rectum

71
Q

Crohn’s Disease

A

Inflammation that commonly affects the small intestine and upper part of large intestine
- Affects women more

72
Q

Sulfasalazine (Treatment of Crohn’s)

A
  • Pro drug activated by bacteria in colon resulting in…
  • 5-ASA Mesalamine = produces local anti-inflammatory effects by blocking arachidonic acid metabolites (NSAIDS)
  • Sulfapyridine = causes systemic anti-inflammatory effects with side effects (photosensitivity, low urine output, kidney stones, dehydration

NURS 316 (5 decks)

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