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Pathophysiology > Ch. 22 & 23 (TEST #3) > Flashcards

Ch. 22 & 23 (TEST #3) Flashcards

1
Q

What upper respiratory viruses in adults are does she discuss?

A

Common cold (several viruses)

rhinosinusitis

influenza

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2
Q

What are some things that URTI can do to our airway?

A

can damage bronchiole epithelium

obstruct airways

lead to secondary bacterial infections

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3
Q

What is some information she gave us about the common cold?

A

it can be caused by several different viruses

    • rhinovirus (most common from ages 5-40) many types
    • para-influenza virus
    • RSV (respiratory syncytial virus)
    • corona virus
    • adenovirus

They are self-limiting in that they last about 7 days

They are mainly transmitted through droplets

URTI

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4
Q

How many common colds do most adults get a year?

Children?

A

2-4

up to 12 a year! (especially if in daycare)

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5
Q

What is the most common vector of the droplet transmission of the common cold?

A

The finger

THIS IS WHY HANDWASHING IS SO IMPORTANT (IT IS THE BEST WAY OF PREVENTION)

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6
Q

What is the most common portal of entry for the common cold?

A

nasal mucosa or conjunctiva of the eye

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7
Q

Would children be considered a major reservoir for the common cold?

A

YES YES YES

THEY SPREAD IT LIKE CRAZY

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8
Q

What are some of the manifestations of the common cold?

A

sore/scratchy throat

rhinorrhea (runny nose)

nasal congestion

sneezing

hoarseness (a big indicator that its just a virus)

HA (headache)

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9
Q

What are the viruses that cause the common cold again?

A

rhinoviruses

parainfluenza viruses

RSV (respiratory syncytial virus)

corona viruses

adenoviruses

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10
Q

For each virus of the common cold, who might get them and what seasons?

A

Rhinovirus - occur late spring and early fall between ages of 5-40

Parainfluenza viruses - occur in children younger than 3

RSV (respiratory syncytial virus) - occur in winter and spring in children younger than 3

corona viruses and adenoviruses - occur in winter and spring

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11
Q

Why do a lot of children with RSV infections get hospitalized?

A

They like to swell the airways and wheezing, basically causes some more serious breathing issues with children

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12
Q

What is another name for rhinosinusitis?

A

sinusitis

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13
Q

What is sinusitis (rhinosinusitis)?

A

Inflammation of the paranasal sinuses and the nasal passages

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14
Q

What is rhinitis?

A

inflammation of the nasal passages

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15
Q

What are your paranasal sinuses?

A

frontal (above the eyebrow)

ethmoid (on the upper bridge of nose and on each side by the inner eye corner)

maxillary (where your cheekbones are)

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16
Q

What is happening with rhinosinusitis?

A

Can be caused by an infection or allergy that obstructs sinus drainage

The passageway (osteomeatal complex) that lets the sinuses drain is narrowed. ALL OF THE SINUSES COME TOGETHER AT THIS POINT TO DRAIN

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17
Q

What happens if our turbinates are swollen while are sinuses are trying to drain?

A

It will be redirected and will go down our throat

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18
Q

Describe the manifestations of acute and chronic rhinosinusitis.

A

Acute (usually caused by rhinovirus 95% of cases): facial pain (behind eyes, between eyes), HA, purulent nasal discharge (thick), decreased sense of smell, fever, even tooth pain DONT USUALLY NEED AN ANTIBIOTIC, USUALLY GOES AWAY ON ITS OWN IN THE ACUTE STAGE (7-10 days)

Chronic: nasal obstruction, fullness in the ears, postnasal drip, hoarseness, chronic cough, loss of taste AND smell, unpleasant breath, HA, AT THIS STAGE ANTIBIOTICS MIGHT BE GIVEN, ESPECIALLY IF SYMPTOMS PERSIST OR WORSEN

SHE ALSO SAYS THAT THE SYMPTOMS OF CHRONIC THAT ARE SHOWN IN THE BOOK ARE SEEN IN ACUTE, SO THEY MIGHT NOT BE THE BEST WAY TO DIFFERENTIATE THEM

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19
Q

What are some other viruses that can cause rhinosinusitis?

A

H influenza

strep pneumonia

moraxella

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20
Q

What is another name for influenza?

A

The flu

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21
Q

Can influenza affect both the upper and lower respiratory tract?

A

YES YES YES

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22
Q

Does the influenza virus mutate every year?

A

YES YES YES

A NEW VACCINE IS CREATED EVERY YEAR

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23
Q

Do people still die from influenza?

A

YES, approximately 36,000 people in the US (especially elderly)

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24
Q

How can influenza be transmitted?

A

by aerosol (3 or more particles) or direct contact

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25
Q

What are the 3 types of infections influenza can produce?

A

it can cause an URTI which is called rhinotracheitis which is like a commoncold but with really bad malaise (often very tired)

Viral pneumonia: fever, tachypnea, tachycardia, cyanosis, hypotension

Respiratory viral infection followed by a bacterial infection OFTEN SAME BACTERIA THAT CAUSE SINUS INFECTIONS (kills the cells that line the LRT, promoting bacterial adhesion)

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26
Q

What is a usual symptom of influenza?

A

a runny nose (virus kill mucous secreting cilliated epithelial cells)

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27
Q

Do we treat influenza with an antiviral?

Can we treat them if they have had heavy exposure even before they show symptoms?

A

YES

YES

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28
Q

How long is the incubation period for influenza?

A

1-4 days

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29
Q

How long are you infectious when you have the flu (normally)?

A

from the 1st day of symptoms to five days

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30
Q

What are the distinguishing features of influenza?

A

A very very sudden onset of malaise and a fever >101

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31
Q

What can help prevent infection of influenza?

A

VACCINATION

THE LAST FEW YEARS OF VACCINATIONS ALSO HAD SWINE FLU IN THEM

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32
Q

What are some symptoms of influenza?

A

fever, chills, rhinorrhea, malaise (pronunced), muscle aching (pronounced), headache, nonproductive cough, sore throat

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33
Q

What are the different types of pneumonia?

A

typical (bacterial)

atypical (viral, mycoplasmal)

community acquired (viral or bacterial)

hospital acquired

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34
Q

What is pneumonia a general term for?

A

Inflammation of the lung tissue

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35
Q

Go more in depth about typical pneumonia.

A

Bacterial

There is inflammation and fluid exudation into the alveoli (impairs gas exchange)

Characterized by purulent sputum

We will have an elevated WBC count (leukocytosis)

Also will show lobar consolidation on x-ray

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36
Q

Go more in depth about atypical pneumonia.

A

Viral or mycoplasmal

“Walking pneumonia”

Inflammatory changes are confined to the alveolar septum and interstitium of the lung (not in the alveoli itself, so it doesnt get into bronchioles)

There will be a lack of alveolar infiltration and purulent sputum

They will have leukocytosis as well as lobar consolidation on x-ray

STILL MAKES GAS EXCHANGE DIFFICULT EVEN THOUGH THE ALVEOLI THEMSELVES ARENT INFILTRATED, IT WILL EFFECT THE VESSELS GOING TO THEM MORE THAN ANYTHING

GAS EXCHANGE IS MOSTLY BETTER WITH THIS TYPE OF PNEUMONIA (IN YOUNGHEALTHY ADULTS O2 SATS MAY NOT DROP TOO MUCH (SHE GAVE EXAMPLE OF GOING FROM 99 AND DROPPING TO 97%)

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37
Q

Go more in depth about community acquired pneumonia.

A

can be either typical or atypical

mostly caused by streptococcus pneumonaie

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38
Q

Go more in depth about hospital acquired pneumonia.

A

can be either typical or atypical

ASPIRATION PNEUMONIA

can be caused by many bacteria (pseudomonas, staph aureus, enterobacter, klebsiella, E. coli)

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39
Q

What is the most common cause of typical community acquired pneumonia (a type of acute bacterial pneumonia as well)?

A

Streptococcus pneumonaie (causes pneumococcal pneumonia)

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40
Q

What makes the virulence of streptococcus pneumonaie so high?

A

It in encapsulated so it has a high resistance to phagocytosis (this delays the antigen presenting process therefore delaying an adaptive immune response)

BY THE TIME WE CAN MOUNT THE APPROPRIATE RESPONSE IT HAS ALREADY INVADED A LOT AND CAUSED A LOT OF SYMPTOMS AND PROBLEMS

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41
Q

What are some factors of pneumococcal pneumonia that make its signs and symptoms vary?

A

How large the lobe is that has been affected

Really just how much damage has been done

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42
Q

Can we live on one lung, why is that important to pneumonia?

A

YES

SO THERE WOULD NEED TO BE A LOT DAMAGE OR WE WOULD NEED TO REQUIRE A LOT OF OXYGEN FOR PNEUMONIA TO BE DETECTED (SOMEONE WITH UNHEALTHY LUNGS OR A WEAK HEART WILL HAVE IT DETECTED EASIER)

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43
Q

What is another disease that can cause acute bacterial pneumonia?

A

Legionnaires Disease

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44
Q

Go more in depth abut legionnaires disease.

A

Caused by legionella pneumophilia

In addition to symptoms of pneumonia it causes diarrhea, hyponatremia, and confusion (involves CNS)

FOUND IN WARM STANDING WATER

THIS CANT BE SPREAD FROM PERSON TO PERSON

CAN BE CONFIRMED THROUGH A URINARY ANTIGEN TEST

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45
Q

What are mycoplasmas?

A

These are the smallest free-living agents of disease that have characteristics of both bacteria and viruses ( FUN FACT: they dont have a cell wall so antibiotics that target cell wall synthesis dont affect them)

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46
Q

What is the most common form of viral pneumonia?

A

influenza

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47
Q

What are the stages of pneumococcal pneumonia?

A

We have inhalation or aspiration (NOT RELATED TO GI ASPIRATION PNEUMONIA) of streptococcus pneumonaie

The bacteria adheres to the alveolar macrophages and show them its cell wall components

This then trigger an inflammatory response

    • attraction of neutrophils
    • release of inflammatory mediators
    • accumulation of fibrinous exudate, RBCs, and bacteria

Then Red hepatization (she doesnt say much about red hepatization in lecture) and consolidation of lung parenchyma (the functional part of the lungs)

There is more leukocyte infiltration (neutrophils and macrophages)

There is now gray hepatization (again, she didnt really talk about it).. and deposition of fibrin on the pleural surfaces, and phagocytosis within the alveoli

Resolution of the infection (becuase we can finally mount an immune response): macrophages in alveoli ingest and take away the degenerated neutrophils, fibrin, and bacteria.

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48
Q

What are the general signs and symptoms of pneumonia (any pneumonia)?

A

We get the signs and symptoms of systemic inflammation: malaise, chills and fever, also we have a productive cough with serous exudate, eventually blood tinged sputum and pleuritic pain, diminished breath sounds over consolidated area and dullness over consolidated area on percussion

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49
Q

So the general steps of pneumonia starting with infection are what?

A

Infection => inflammation => serous exudate => fibrous exudate (red hepatinization, consolidation, consolidation causes decreased breath sounds in that area and dullness in percussion) => gray hepatinization (the WBCs denature hemoglobin) => WBCs destroy fibrous proteins (that are causing consolidation) and liquefy exudate (which is reabsorbed into circulation=> resolution

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50
Q

What is an interesting statistic she gives about tuberculosis and death?

A

It is the worlds foremost cause of death from a single infectious agent

causes 26% of avoidable deaths in developing countries

ALSO #1 CAUSE OF DEATH IN PEOPLE WITH HIV

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51
Q

Does TB have many drug resistant forms that are hard to treat?

A

YES YES YES

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52
Q

What environment does mycobacterium tuberculosis hominis thrive in?

A

an O2 rich environment (its an aerobic bacteria)

THIS IS WHY WE MOSTLY SEE IT IN THE LUNGS, BUT IT HAS BEEN SEEN IN JOINT SPACES, SPINE, DEEP SKIN TISSUE, ECT…

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53
Q

What does the tuberculosis bacteria have that makes it resistant?

A

It has a waxy capsule that makes it resistant to destruction and gives it the ability to live outside of the body on a surface for a very long time

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54
Q

What does the capsule of tuberculosis bacteria do to allow us to identify it?

A

It retains the red dye in acid-fast staining

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55
Q

What type of reaction does tuberculosis evoke?

A

Type IV cell-mediated hypersensitivity => chronic inflammation and tissue destruction

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56
Q

How is TB transmitted?

A

inhalation of airborne droplets from infected people

MUCH HIGHER RISK IN CROWDED AND CONFINED LIVING CONDITIONS

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57
Q

Describe primary tuberculosis.

A

PEOPLE WITH PRIMARY TUBERCULOSIS ARE NOT INFECTIOUS (NOT CONTAGIOUS)

ALSO CALLED LATENT TB

THEY USUALLY DEVELOP GHON COMPLEXES (GRANULOMATOUS LESIONS)

THEY CAN STILL GET THE ACTIVE FORM OF TB, BUT THEY HAVE WALLED IT OFF TO STOP IT FROM RUNNING RAMPID

ABOUT 5% OF PEOPLE WITH THIS GO ON TO GET THE ACTUAL DISEASE, NORMALLY BECAUSE THEY HAVE AN INADEQUATE IMMUNE SYSTEM

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58
Q

With the initial TB infection, how long will it take after exposure to develop a positive TB test?

A

3-6 weeks (because of delayed T cell response)

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59
Q

What type of immune response is going on with the initial TB infection?

A

A cell-mediated immune response (macrophages)

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60
Q

What do Ghon complexes contain?

A

macrophages

T cells

inactive TB bacteria

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61
Q

Describe the steps of the primary tuberculosis infection.

A

The bacteria is introduced to the body

We have a cell-mediated hypersensitivity response (which leads to cell-mediated immunity and gives us our positive TB skin test)

Then we have our granulomatous inflammatory response

leads to ghon complex

which can become a healed dormant lesion

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62
Q

What can the ghon complexes (and healed dormant lesions) do at any time?

A

They can become activated and cause progressive or disseminated tuberculosis (this is when they show symptoms and are infectious)

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63
Q

What is another way that someone with primary tuberculosis can become infectious and show symptoms?

A

They could be reinfected by being exposed again.

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64
Q

What is miliary TB?

A

This is tuberculosis that can go to any tissue

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65
Q

So with primary TB we usually isolate the bacteria in Ghon foci so the bacteria are inactive and we arent contagious, but what is we cant mount a good enough immune response?

A

The bacteria will continue to multiply in the lungs and will become progressive primary TB

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66
Q

Why do we test people for latent TB (inactive) before we do transplants?

A

If someone has latent TB and we suppress their immune system for transplantation the bacteria can become active because our immune system couldnt keep it walled off.

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67
Q

What does the TB skin test look for?

A

It is measuring the delayed hypersensitivity that follows exposure (T cells)

  • result means they werent exposed or that they were exposed but not infected (can get false negative if tested too early, 3-6 weeks (or even 12 weeks) for response)

+ means they were exposed and infected and the cell-mediated immune response was initiated

SKIN TEST JUST SHOWS IF THEY HAVE BEEN EXPOSED AND INFECTED (DOESNT DIFFERENTIATE BETWEEN LATENT AND ACTIVE)

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68
Q

What is the pointof a chest x-ray in diagnosing TB?

A

These identify Ghon lesions (inactive) or cavitaties (if active)

IF CAVITATIES ARE SEEN THE PATIENT WILL BE PUT INTOISOLATION UNTIL THEY GET SPUTUM CULTURE AND ACID-FAST STAIN RESULTS BACK

CAN DIFFERENTIATE BETWEEN ACTIVE AND INACTIVE FORM

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69
Q

What is the point of a sputum culture and acid-fast stain in relation to TB?

A

These are required for the definitive diagnosis of active TB infection

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70
Q

How long is the treatment for TB

A

6-12 months

because it is so long we often get compliance issues which leads to drug resistant forms

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71
Q

What cancer is the leading cause of death of all the cancers?

A

lung cancer

only 13-15% have a 5 year survival rate

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72
Q

What type of lung cancer arises from the epithelial linings of the lungs?

A

bronchogenic carcinoma

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73
Q

What are the different types of bronchiogenic carcinomas?

A

small cell

non-small cell

    • large cell carcinoma
    • squamos cell
    • adenocarcinoma
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74
Q

Go more in depth about the different types of bronchiogenic carcinomas.

A

Small cell (20-25%)

  • more common in men than women
  • strongly associated with smoking
  • highly malignant (likes to metastasize to the brain)
  • 70% have metastasized by time of diagnosis

Squamos cell (25-40%)

    • most common in men
    • closely correlated with smoking history

Adenocarcinoma (20-40%)

    • most common type in north america and in women and nonsmokers
    • tend to be located peripherally (on the outside

Large cell (10-15%)

    • highly anaplastic and metastatic
    • poor prognosis

NONE OF THESE REALLY HAVE A GOOD PROGNOSIS

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75
Q

What are some things that affect the manifestations of lung cancer?

A

– the changes in organ function (organ damage, inflammation, and failure)

– local effects of tumors (compression of nerves or veins, GI obstruction) remember its near the esophagus and stomach

– ectopic hormones secreted by tumor cells (paraneoplastic syndrome)

– nonspecific signs of tissue breakdown (protein wasting, bone breakdown)

MOSTLY LIKE TO PRESENT AS CHRONIC COUGH

ALSO CAN HAVE SOA, WHEEZING, COUGHING UP BLOOD (INVASION INTO BLOOD VESSELS), PAIN (TUMOR COMPRESSING NERVE), HOARSNESS (COMPRESSION OF LARYNGEAL NERVE), SWALLOWING ISSUES (ESOPHAGEAL COMPRESSION), PLEURAL EFFUSION (TUMORS SECRETING EXUDATES), ATELECTASIS, PROFOUND BREATHING ISSUES IF IT MAKES IT TO LARGER AIRWAY

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76
Q

Where is the snoring zone in kids and what could cause snoring?

A

In the naso and oropharynx

from the tongue being pushed back or nasal cavities being swollen shut

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77
Q

Where is the inspiratory stridor zone in kids and what would be affected if swollen?

A

basically at the top of the trachea down to the bottom of the thyroid cartilage (larnygeal area)

if swollen this will affect voice quality, you will be able to hear yourself wheeze when you talk (hoarsness, viral symptom most often)

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78
Q

Where is the expiratory stridor zone in kids and what would be affected here if swollen?

A

Bottom of thyroid cartilage down to where trachea splits

This area will affect cough quality is swollen (irritative symptom)

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79
Q

Where will you mostly hear wheezing?

A

Way down in the lower airways, in the smaller bronchioles.

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80
Q

When do alveoli fully develop in infants?

A

37 - 40 weeks gestation

premmature infants often have respiratory issues

81
Q

How does the smaller size of childrens airways affect our thinking of respiratory issues with them?

A

Their airways are much smaller so they cant handle as much swelling or obstructions in their airways

82
Q

Is a childs chest wall very compliant?

A

YES, this is a good thing

but if this is affected we could have major issues

83
Q

What are retraction in relation to ventilation with children?

A

This is where instead of the chest expanding on inspiration you will see in the intercostal spaces they will be sucked in on inspiration

84
Q

So is the airway of a child under more resistance? why?

Why is this important to know?

A

YES, because they are a smaller diameter.

because of the smaller radius, if they have increases in mucous or more obstructions that change the diameter there will need to be an increase in pressure to move air and the flow rate decreases

85
Q

In regards to airway obstructions in children, what will we be able to assess with the increase in airway resistance?

A

Extrathoracic airways (upper): Seen with croup

  • prolonged inspiration => inspirational stridor
  • Inspiratory retractions (ribs are moved outward while body wall stays put)
  • nasal flaring

Intrathoracic airways (lower): seen with bronchial asthma

  • AIR TRAPPING:
  • prolonged expiration => wheezing
  • Rib RETRACTIONS trying to force the air out (ribs are pulled inward, but air does not leave the lungs)

EXPIRATORY WHEEZING WITH BRONCHIAL ASTHMA IS OFTEN THE FIRST SIGN (NEED INTERVENTION QUICK), THEN COMES THE INSPIRATORY WHEEZE AND EVENTUALLY WHEN NOT ENOUGH AIR CAN BE MOVED THERE WILL BE NO WHEEZING

86
Q

What is another name for respiratory distress syndrome?

A

hyaline membrane disease

87
Q

When do infants usually present with signs of respiratory distress syndrome?

A

usually within the first 24 hours of life

MOST COMMON CAUSE OF RESPIRATORY DISEASE IN PREMATURE INFANTS

88
Q

what part of the respiratory system is developed first in a fetus?

A

their conducting airway

THEN THEY DEVELOP WHATS NEEDED FOR GAS EXCHANGE

89
Q

When do children reach full alveolar development?

A

5 years of age

90
Q

What is going on with respiratory distress syndrome?

A

There is alveolar collapse due to the incomplete development of alveolar type II cells => lack of surfactant (liquid that keeps alveoli from collapsing) THINK ABOUT WHEN TRYING TO INFLATE A BALLOON, IT GETS A LOT EASIER AFTER YOU GET THAT INITIAL BUBBLE IN THERE, THE SURFACTANT IT THAT FIRST BUBBLE => infants arent strong enough to inflate their alveoli (think about surfactants role with alveoli)

Protein-rich fluids also leak into the alveoli and block oxygen uptake even more

91
Q

How is hyaline membrane disease treated?

A

mechanical ventilation (may lead to bronchopulmonary displasia and chronic respiratory insufficiency)

92
Q

What do children with respiratory distress syndrome often present with?

A

central cyanosis

chest wall retraction

fatigue from increased work of breathing

decreased appetite

Cant breastfeed

93
Q

Describe the steps of respiratory distress syndrome.

A

premature birth => decreased surfactant and immature lung structures => decreased lung compliance => atelectasis => hypoxia => pulmonary vascular constriction and increased pulmonary capillary permeability => pulmonary hypertension and movement of capillary n?fluid into alveoli => decreased pulmonary perfusion and hyaline membrane deformation (further decreases lung compliance)

94
Q

What are two common upper and one lower respiratory tract infections in children?

A

Upper: croup (usually runs its course) & epiglottitis (most dangerous)

Lower: acute bronchiolitis (if severe need intervention)

ALL OF THESE CAN LEAD TO INFLAMMATION AND EXUDATE SO THE SMALLER THE AIRWAY THE LARGER THE RISK

95
Q

Go more in depth about croup.

A

Also called acute laryngotracheobronchitis

common from 3 months - 5 years

mostly caused by parainfluenza (75%) also can be caused by influenza A or RSV

causes subglottic edema

usually occurs after an episode of rhinorrhea, sore throat and fever

Most common form of acute respiratory obstruction in children.

usually benign and self limited

kids under a year old with this need more worry

INSPIRATORY STRIDOR AND BARKY COUGH (ESPECIALLY IN EVENING)

Can be treated with steam or a inhaler (nebulized epinephrine) if severe, but not usually treated

96
Q

Go more in depth about epiglottitis.

A

Rapidly progressive and life-threatening

High risk for airway obstruction

Most often caused by the H. influenza type B (HIB) VACCINATION AGAINST THIS NOW AND DAYS

needs to be caught immediately

97
Q

Go more in depth about acute bronchiolitis.

A

Viral infection of lower airway

most commonly caused by RSV

high risk for respiratory failure secondary to impaired gas exchange

hard to get air out

generally from 2 years and younger:

high danger for under 1 year of age (smaller airway)

very very high under 6 months of age (smaller airway)

EXPIRATORY WHEEZING (FROM BRONCHOSPASM, MUCOSAL INFLAMMATION AND EDEMA)

Usually just supported through the infection for treatment

98
Q

What are the manifestations of epiglottitis?

A

High fever

sore throat (may not be able to verbalize because of young age, might not be eating well)

Inspiratory stridor

severe respiratory distress

99
Q

What is the treatment for epiglottitis?

A

emergency airway (rapidly progressive and can swell airway shut) and antibiotics

100
Q

What does the abbreviation SIDS stand for?

A

sudden infant death syndrome

101
Q

Go more in depth about sudden infant death syndrome.

A

Unknown cause

Age of incidence: lower during first month, increases in second month, peaks in the 3rd and 4th months of life

more common in male infants

There is a possible seasonal variation (possible relationship with respiratory infections)

HUGE range of risk factors

102
Q

In cyanosis an early or late sign?

A

LATE

103
Q

What is the difference between central and peripheral cyanosis?

A

central = buccal mucosa, tongue, and lips

peripheral = nail beds

104
Q

What is clubbing caused by?

A

chronic diseases that interfere with oxygenation

105
Q

Is dyspnea objective?

A

NO

this is a subjective sensation of SOA or difficulty breathing

106
Q

What can a dry cough indicate?

A

tumor

congestion

hypersensitive airway

107
Q

What can a productive (wet) cough indicate?

A

infection

108
Q

What are the two mechanisms of respiration?

A

ventilation and perfusion

109
Q

What is ventilation?

A

the movement of air in and out of the lungs

110
Q

Where is our respiratory center?

A

medulla oblongata (pacemaker of respiration)

stimulates autonomic breathing

111
Q

What nerve innervates the diaphragm and intercostals?

A

the phrenic nerve

112
Q

Which nervous system controls bronchodilation (PNS OR CNS)?

A

CNS (only responds to oxygen needs)

113
Q

What do chemoreceptors do in regards to respiration?

A

sense the O2 levels, CO2 levels, and pH of blood (carotid and aortic bodies)

can adjust rate and depth of respiration

114
Q

What do motion receptors do in regards to respiration?

A

They sense movements of muscles to change the rate and depth of our breathing to supply our oxygen demand

115
Q

What is perfusion and what does it require?

A

perfusion is the blood supply to the alveoli and the gad exchange that occurs

requires:
alveolar sacs - require surface area (mucous or swelling lose surface area, also pulmonary edema from left sided heart failure)

surfactant

hemoglobin (anemia, hypovolemia, right sided heart issues can affect this)

116
Q

What are some things that can impair diffusion?

A

The thickness of the respiratory (alveolar-capillary) membrane

    • increased thickness = decreased perfusion
    • inflammation and edema can cause this

Decreased surface area of alveoli available for gas exchange

    • decreased surface area = decreased gas exchange
    • atelectasis (consolidation is a large area of atelectasis), pleural effusion, pneumothorax, emphysema can affect this

Gradient or the difference in partial pressure of gases in alveoli and blood
– decreased gradient = decreased gas exchange

– high altitudes and hypoventilation => hypoxemia but not hypercapnia

– PO2 in alveoli > capillary PO2 needed to move O2 into capillary

PCO2 capillary > PCO2 alveoli needed to move CO2 from capillary to alveoli

117
Q

What is v/q ratio?

A

ventilation/perfusion ratio

118
Q

What is happening with a low v/q ratio with?

A

We have impaired ventilation which causes a loss of inflated surface area on alveoli which impairs gas exchange in that area

NO IMPAIRMENT OF BLOOD FLOW TO AREA

119
Q

What is happening with a shunt (very low) v/q?

A

we would have a totally block off area that collapses the alveoli further down that part of the airway which gives us a massive decrease in surface area of alveoli for gas exchange

NO IMPAIRMENT OF BLOOD FLOW TO AREA

120
Q

What is happening with a high v/g?

A

A blockage of the blood flow to the alveoli (for example a pulmonary embolus) which affects perfusion to that area

NO IMPAIRMENT OF VENTILATION OF ALVEOLAR SURFACE AREA

121
Q

What are some causes of respiratory failure?

A

hypoventilation => hypercapnia, hypoxia

    • depression of respiratory center (head injury, drugs)
    • diseases of respiratory nerves or muscles
    • thoracic cage disorders

Ventilation/perfusion mismatching

Impaired diffusion => hypoxemic but not hypercarbic (normal CO2 levels)

    • interstitial lung disease
    • ARDS
    • pulmonary edema
    • Pneumonia
122
Q

What PO2 (arterial blood gas) and sat levels are considered hypoxemic?

A

PO2

123
Q

What are some early, late, and chronic signs of hypoxemia?

A

Early: anxiety and restlessness

Late: cyanosis

Chronic: clubbing

124
Q

What issues can cause hypoxemia?

A

not enough oxygen in the air

respiratory system issue

neuromuscular or muscular issue

circulatory issue

125
Q

What are the compensatory mechanisms our SNS will put in place with hypoxemia?

A

Increase RR

Increase HR

Increase contractility of heart

Vasoconstrict

126
Q

If hypoxemia goes on for long, what neuro changes can we see (behaviors)?

A

agitated or combative behavior

euphoria

impaired judgement

convulsions

delirium

stupor

coma

127
Q

What are some other problems with vital areas we can see if hypoxemia goes on for long? (3 things)

A

Retinal hemorrhage

hypotension and bradycardia

128
Q

At the PCO2 level are we considered to be hypercapnic?

A

PCO2 > 50 mm hg

129
Q

With hypercapnia what state are we in?

A

respiratory acidosis

130
Q

What manifestations occur with hypercapnia?

A

vasodilation => HA, conjunctival hyperemia, warm flushed skin

131
Q

What are some causes of hypercapnia?

A

decreased respiration

Decreased nerve firing

    • carbon dioxide narcosis
    • coma
    • disorientation
    • somnolence

Decreased muscle contraction

132
Q

What can chronic CO2 elevation do to our chemoreceptors?

Why is this important?

A

Bicarb neutralization of chemoreceptors

THIS RELATES TO COPD PATIENTS:

THE CO2 MESSAGES TO CHEMORECEPTORS WILL BE IGNORED, SO ONLY THE OXYGEN LEVELS WILL BE LOOKED AT

THIS IS WHY COPD PATIENTS HAVE A HYPOXEMIC DRIVE, SO THE SLIGHTLY LOW OXYGEN LVLS ARE WHAT STIMULATE THEM TO BREATH WHICH IS WHY WE NEED TO BE CAREFUL WHEN GIVING THEM OXYGEN

133
Q

Name the layers of the pleura from the outside in.

A

parietal pleura (lines thoracic wall and superior diaphragm)

pleural cavity (contains thin layer of serous fluid to prevent friction)

Visceral pleura (covers the lung)

134
Q

So what part of respiration do pleural disorders affect?

A

ventilation

if they get severe enough and collapse airways they can affect perfusion

135
Q

What is another name for pleuritis?

A

pleurisy

136
Q

What is pleuritis?

A

Inflammation of the pleura

COMMON IN INFECTIOUS PROCESSES

137
Q

What is an audible finding that is indicative of pleuritis?

A

pleural friction rub (sounds like hair rubbing together

best heard on inspiration

138
Q

What ca pleuritis be an indicator of?

A

Cancer

139
Q

What is a common sign of pleurisy?

A

pleural pain

140
Q

Describe the onset and location of pleurisy.

A

Sudden onset

usually unilateral

localized to the lower and lateral parts of the chest

141
Q

When is the pain of pleuritis exacerbated?

A

Chest movement::

deep breaths

coughing

laughing

142
Q

How can we differentiate pleural pain from musculoskeletal, bronchial irritation, myocardial pain?

A

Musculoskeletal: usually bilateral, inferior portions of rib cage, EXACERBATED BY CONTRACTION OF ABDOMINAL MUSCLES

Bronchial irritation: substernal and dull rather than sharp, worse with coughing, not affected by deep breathing

Myocardial: substernal, sharp, radiates, not affected by respiratory movements

143
Q

What is a pleural effusion?

A

Abnormal collection of fluid in the pleural cavity.

144
Q

What are some things that can cause a pleural effusion?

A

`Hydrothorax: serous transudate (common cause is CHF because of increased capillary pressure

Empyema: Pus (can be caused by direct infection of pleural space from adjacent bacterial pneumonia, abscess rupture, trauma (increased capillary permeability)

Chylothorax: lymph fluid (trauma, inflammation, malignant infiltration (most common)

Hemothorax: blood (trauma, vessel rupture, surgical complication)

145
Q

In the area of the effusion what would we auscultate and percuss?

A

Dullness on percussion and diminished breath sounds

146
Q

Will someone with pleural effusion become hypoxic?

A

Yes, mildy

147
Q

What is a pneumothorax?

A

This is when air enters the pleural cavity.

CAN CAUSE A PARTIAL OR COMPLETE COLLAPSE OF LUNG

148
Q

What are the two types of pneumothorax?

A

Spontaneous (usually tall skinny athletes)

CAN BE RUPTURE OF AIR FILLED BLISTER ON LUNG OR SOMETHING TO DO WITH PRESSURE DIFFERENTIALS

Traumatic (through chest injuries)

    • open
    • tension
149
Q

What is an open pneumothorax (traumatic)?

A

This is when air enters the cavity through the wound on inhalation and leaves on exhalation

150
Q

What is a tension pneumothorax?

A

Air enters the pleural cavity through the wound on inhalation but cant exit on exhalation

151
Q

So if the lung is being compressed by any fluid or air what do we usually do?

A

Put in a chest tube to drain whatever it is.

152
Q

What is going on with the differences in pressure with a spontaneous pneumothorax?

A

alveolar pressure > pleural pressure so atmospheric air is being pushed into the pleural space

AIR WILL ACCUMULATE AND BEGIN COLLAPSING LUNG

153
Q

What happens with the pressure in the thoracic cavity when breathing in and out?

A

With an open pneumo, when you breath in air will also come into the hole that caused the injury, thus the lung will not be able to inflate with oxygen, it will get smaller

But when breathing out the air that was in the pleura will escape out the injury, while this is happening the carbon dioxide from the other lung will inflate the collapsed lung a little bit

154
Q

So with a tension pneumo, air come in and cant escape the pleural cavity, is that life threatening? why?

A

YES YES YES

eventually the unaffected lung will become compressed and atelectasis will occur, there will be a mediastinal shift and tracheal deviation towards the unaffected side

The vena cava will become compressed and will affect venous return to the heart.

155
Q

Does the size of the pneumothorax and the integrity of the underlying lung affect the manifestations of it?

A

YES YES YES

156
Q

What are some manifestations of a pneumothorax?

A

ipsilateral chest pain

immediate increase in respiratory rate accompanied by dyspnea

tachycardia

asymmetry of chest movement

hyperresonance on percussion and decreased breath sounds over the area of pneumothorax

hypoxemia

hypotension (affects venous return)

157
Q

What is atelectasis a general term for?

A

incomplete expansion of a lung or a portion of a lung (the alveoli arent fully expanding)

158
Q

What can cause atelectasis?

A

airway obstruction (mucus plug)

Lung compression (pleural effusion, tumor, anything that occupies space)

increased recoil caused by inadequate pulmonary surfactant (emphysema)

USUALLY SEEN AT BASES

159
Q

What is absorption atelectasis?

A

complete obstruction of an airway is followed by the absorption of air from the dependent alveoli and collapse of that portion of the lung

high risk post-op

160
Q

What is compression atelectasis?

A

This has to do with things that occupy space

Most common with pleural effusions from CHF or cancer

161
Q

How can deep breathing exercises help someone with absorption atelectasis?

A

If one half of the alveoli is plugged, there is a something in the septum between the halves called the closed pore of kohn, if you breath in deep enough air can travel through that pore and inflate the obstructed alveoli which can pop that mucus plug up out of the way

162
Q

What are some manifestations of atelectasis?

A

Increased RR (early)

Increased HR (early)

dyspnea

cyanosis

signs of hypoxemia

Decreased chest expansion and absence of breath sounds on the affected side

intercostal retractions

fever and other signs of inflammation may develop

163
Q

What do obstructive airway disorders cause?

A

Increased resistance to air flow

Characterized by difficult expiration

ITS ALL ABOUT THE EXPIRATION

164
Q

What are some obstructive airway disorders?

A

Bronchial asthma

Chronic (COPD):
chronic bronchitis
emphysema
bronchiectasis
cystic fibrosis
165
Q

Go more in depth about bronchial asthma.

A

chronic inflammatory airway disease (can be more pronounced in childhood)

exaggerated hypersensitivity response to variety of stimuli

5% of population affected

usually spontaneosly reversible or with treatment

There are two types:

extrinsic - type I hypersensitivity
intrinsic - diverse nonimmune mechanism

166
Q

What are the manifestations of bronchial asthma?

A

recurrent episodes of airway obstruction characterized by wheezing, breathlessness, chest tightness, and a cough that is worse at night and early in the morning

167
Q

Go more in depth about extrinsic bronchial asthma.

A

type I hypersensitivity

by far more common that intrinsic

MAST cells, IgE, and eosinophils release inflammatory mediators that causes acute response within 10-20 minutes

There is a late phase that is caused by airway inflammation usually within 4-8 hours (this is why we watch people with reactions like this for a while)

168
Q

What is the process of the early and late phase of extrinsic bronchial asthma reaction?

A

Allergen enters system

MAST cells release mediators (causes bronchospasm) triggered by IgE EARLY PHASE

More WBCs infiltrate and release inflammatory cytokines EARLY PHASE LEADING INTO LATE PHASE (causes airway inflammation)

airway inflammation leads to edema, impaired muccocilliary function, epithelial injury (increase in mucous causes even smaller airway and increased airway responsiveness LATE PHASE

169
Q

Go more in depth about intrinsic (nonatopic) asthma.

A

Causes:
respiratory infections
– cause epithelial damage and IgE production

Exercise, hyperventilation, cold air
– loss of heat and water may cause bronchospasm

Inhaled irritants

  • -smoking
    • causes inflammation and vagal reflex

Aspirin and other NSAIDs
– abnormal arachidonic acid metabolism

170
Q

What are clinical things that happen to people with bronchial asthma?

A

decreased peak expiratory flow rate
– below 50% indicates a need for emergency intervention

hyperinflation and prolonged expiration due to air trapping

Dyspnea and fatigue due to increased work of breathing

hypoxemia and hypercapnea

distant breath sounds

expiratory wheezing may be present (as it is prolonged you can get both inspiratory and expiratory, and eventually you wont hear anything because not enough air is being moved)

pulsus paradoxus
– fall of systolic blood pressure during inspiration due to increased negative intrapleural pressure caused by air trapping

171
Q

What is considered severe asthma?

A

asthma that is refractory to conventional methods of therapy

172
Q

Who is at a higher risk for severe asthma?

A

people with history of previous episodes that resulted in respiratory failure, respiratory acidosis, and the need for intubation (scarring of the lung tissue)

REMEMBER KIDS HAVE MUCH SMALLER AIRWAYS SO THEY ARE AT HIGH RISK

173
Q

Do people with severe asthma rapidly deteriorate during an attack?

A

YES YES YES

174
Q

go more in depth about the COPDs she talked about.

A

emphysema: enlargement of air spaces and destruction of lung tissue

Chronic bronchitis: increased mucous production, obstruction of small airways, and chronic cough

Bronchiectasis: UNCOMMON type of COPD infection and inflammation destroy smooth muscle in airways, causing permanent dilation

175
Q

What are the pathologic machanisms of COPD?

A

Inflammation and fibrosis of bronchial wall stiffen lungs and obstruct airflow

hypertrophied mucus glands = increased mucus production to an excess which obstructs airflow

Loss of elestic lung fibers cause airways collapse, obstructed exhalation, and air trapping HIGH RISK FOR SPONTANEOUS PNEUMO

176
Q

What does recoil have to do with difficult expiration?

A

The elastic fiber help with recoil by pushing the air out of the sac on expiration, having that impaired coupled with a narrowed airway can be a recipe for horrible expiration

177
Q

Go more in depth about emphysema?

A

loss of lung elasticity (ventilation)

The air spaces are enlarged but there is damage to the alveolar sac wall and capillary beds (perfusion)

top two causes: SMOKING

    • neutrophils release trypsin
    • increased neutrophil numbers due to inhaled irritants can damage alveoli

hereditary defect = rare

COPD EFFECTS BOTH VENTILATION AND PERFUSION

178
Q

What are the two types of emphysema and some info about them?

A

Centriacinar: MOST COMMON TYPE
seen predominately in male smokers
involves the central bronchioles of respiratory lobule
the alveolar ducts and sacs are initialy preserved
changes are primarily seen in upper parts of lungs

Panacinar:
initially involves the peripheral alveoli
later extends to involve the more central bronchioles
changes are seen in the lower parts of the lungs

179
Q

What blood gas levels will central chemoreceptors respond to?

A

central = hypercapnia

WITH COPD THE CENTRAL RECEPTORS ARE IGNORED, BECAUSE OF CHRONIC HYPERCAPNIA

180
Q

What blood gas level do peripheral chemreceptors respond to?

A

peripheral = hypoxia

THIS IS THE ONLY TYPE OF CHEMORECEPTOR THE BODY RESPONDS TO WITH COPD

181
Q

Go more in depth about chronic bronchitis.

A

Airway obstruction of major and small airways

hypersecretion of mucus in large airways

Increased goblet cells (secrete mucous) in small airways

fibrosis of bronchial wall (RECOIL DECREASE)

USUALLY PRESENT WITH PRODUCTIVE COUGH FOR 3 CONSECUTIVE MONTHS

MIDDLE-AGED MALE SMOKERS

182
Q

What is the difference between pink puffers and blue boaters?

A

Pink puffers (emphysema):

    • proportionate loss of ventilation and perfusion
    • increase respiration to maintain oxygen levels
    • dyspnea; increased ventilatory effort
    • use accessory muscles; pursed lip breathing

blue bloaters (bronchitis):

    • cant increase respiration enough to maintain oxygen levels
    • cyanosis and polycythemia
  • cor pulmonale (right sided heart failure)
183
Q

What can chronic air trapping cause?

A

barrel chest (AP = transverse)

normally the 2x the AP diameter is equal to the transverse diameter of the chest

184
Q

Go more in depth about bronchiectasis.

A

UNCOMMON

Persistent abnormal dilation of the bronchi

infection and destruction of bronchial walls

pooling of secretions produces vicious cycle of chronic inflammation and development of new infections

OBSTRUCTIVE:
confined to segment of lung distal to a mechanical obstruction
tumors, foreign bodies, mucus plugs

NONOBSTRUCTIVE:
localized and generalized
usually bilateral and affects lower lobes

185
Q

What information did she give about cystic fibrosis?

A

Recessive disorder in chloride transport proteins
– high concentrations of NaCl in sweat

Mucus is thicker (less NA and water in respiratory mucus)

    • obstructs airways
    • obstructs pancreatic and biliary

Often get cholithiasis and pancreatitis, steatorrhea and diarrhea

186
Q

What is a first sign of this disease at birth?

A

babies will get constipated because of there thick thick mucous.

OFTEN HAVE GI PROBLEMS AS WELL AS RESPIRATORY PROBLEMS BECUSE OF THICK SECRETIONS

187
Q

What is diffuse parenchymal lung disease?

A

This is a restrictive disorder NOT OBSTRUCTIVE

affects the collagen and elastic tissue of alveolar walls, airway arteries/veins

slow onset

destroys type I alveolar cells so type II cells take over and usual trigger inflammation

MANY DIFFERENT TYPES (100) (pulmonary fibrosis and sarcoidosis for example)

INHALATION PROBLEMS, LUNG COMPLIANCE

188
Q

What are the manifestations of diffuse parenchymal lung disease?

A

tachypneic

dyspnea with exercise

decreased lung volumes

189
Q

What are some disorders of pulmonary blood flow that she discussed?

A

Pulmonary embolism

pulmonary hypertension
– primary: blood vessel walls thicken and constrict

– secondary: elevation of venous pressure, increased pulmonary blood flow, pulmonary vascular obstruction, hypoxemia

190
Q

What can cause a pulmonary embolism?

A

thrombus (blood)

air embolus (iv infusion)

fat embolus (from bone marrow post fracture)

DVT IS MOST COMMON SOURCE OF PULMONARY EMBOLI

191
Q

What are the sign and symptoms of a pulmonary embolus?

A

chest pain

dyspnea

tachypnea

CAN CAUSE BRONCHOCONSTRICTION

192
Q

What is pulmonary hypertension?

A

Elevated pressure in the pulmonary vascular system

193
Q

What are some secondary causes of pulmonary HTN?

A

elevation is left atrium pressure

increased pulmonary blood flow

increased pulmonary vascular resistance

obstruction to pulmonary blood flow

THE PULMONARY VESSELS ARE MORE COMPLIANT (EVEN THE ARTERIES TO A POINT)

194
Q

What happens with early and late pulmonary HTN (to the vessels)?

A

early: hypertrophic mucular layer

Late: internal fibrosis (thick inner fibrous layer, decreases ability to change diameter)

195
Q

What is cor pulmonale?

A

This is right sided heart failure secondary to respiratory disease
mechanism:
decreased lung ventilation => pulmonary vasoconstriction => increased workload on the right heart => decreased oxygenation =>
kidneys release erythropoietin => more RBCs made => polycythemia makes blood more viscous => increased workload of heart

196
Q

What is ARDS (acute respiratory distress syndrome)?

A

cause: acute lung injury

exudate enters alveoli

    • blocks gas exchange
    • makes inhalation more difficult

This leads to neutrophils entering the alveoli

    • release more inflammatory mediators
    • release proteolytic enzymes
197
Q

What are the manifestations of ARDS?

A

severe dyspnea

hypoxemia

pulmonary infiltrates

HIGH MORTALITY RATE 35-60%

198
Q

What are some causes of ARDS?

A

aspiration of gastric contents

major traumas

sepsis

pancreatitis

drug reactions

alcohol abuse

USUALLY DEVELOPS 8-12 HOURS AFTER INITIATING INJURY

199
Q

Explain the pathogenesis of ARDS.

A

Acute lung injury => alveolar injury and capillary injury => type II alveolar damage and inflammatory response => decreased surfactant production and increased capillary permeability => atelectasis, decreased compliance, and edema

ALSO MICROTHROMBI (FROM PLATELET AGGREGATION) INCREASE THE PULMONARY HYPERTENSION AND WELL AS FRIBROBLAST GROWTH FACTORS CAUSE PULMONARY FIBROSIS

Pathophysiology (13 decks)

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