Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Path Exam 1 > Exam 2 Respiratory > Flashcards

Exam 2 Respiratory Flashcards

1
Q

respiratory system

A

RS = Nose > pharynx > larynx > trachea > bronchi > bronchioles > lungs

Nose reaches blood vessels

Ex: winter time > dry nose > prone to nose bleeds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

nose and blood vessels

A

Nose reaches blood vessels

Ex: winter time > dry nose > prone to nose bleeds

Inhale > moisten and warm the air > why it reaches blood vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

volume of oxygen dissolved in the plasma

A

varies directly with the partial pressure of oxygen in the arteries

if the pressure of oxygen in the arterial blood (PO2) is within 90-100 mmHg, Hgb is maximally saturated with oxygen > tissues remain oxygenated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

process of gas exchange

A
  1. Air enters to the alveolus on inspiration > air moves across the alveolar membrane > to the RBC
  2. At the same time > carbon dioxide moves from the RBC > to the alveolus > excreted during expiration

Summarized = Air we inhale goes to alveoli > air gets diffused into the capillaries > CO2 from capillaries gets diffused into the alveoli > gets exhaled

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

alveoli / Function

A

thin-walled/ballon-like structure surrounded by pulmonary capillaries

oxygen (now in the blood) combines with the heme (part of hemoglobin) to form oxyhemoglobin

from lungs and goes to L atrium > L ventricle > to rest of body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

clinical implication: O2 saturation

A

oxygen saturation of hemoglobin (blood) is measured by pulse oximeter

O2 stat machine = use pulse oximeter

ex: nasal cannula > 92% RA w/ 2L NC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Perfusion

A

movement of blood through pulmonary circulation

ventilate in order to perfuse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

diffusion

A

transfer of gases btw alveoli and pulmonary capillaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

V-Q ratio (ventilation-perfusion ratio)

A

ratio of air reaching alveoli to amount of blood reaching alveoli

V and Q are equal when they are both matching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

shunt

A

Perfusion no ventilation

  • blockage to prevent O2 from reaching blood
  • ANY respiratory disorders can cause this (secretions or blockage) or anything that would restrict air from reaching
    ex: pneuomnia, PE, Reduction of secretion
  • fluid in lungs/mucous - air present but cannot reach to area due to block
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

dead space

A

Vent no perfusion

no blood reaching area due to blockage

O2 reaches to the area but no blood flow

ex. Blood clot in pulm artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

V-Q mismatch (ventilation-perfusion ratio)

A

when air cannot flow into alveoli or blood flow is altered to alveoli

Ex. PE: blood clot preventing delivery of blood to complete gas exchange

airway obstruction: blocked and cannot pass through > less oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hypercapnia Normal “main” stimulus to breathing

A

pons and medulla = respiratory center

sensitive to high CO2 levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

hypoxic drive

A

Becomes the trigger for breathing

ex: case to individuals with COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

chronic elevation of CO2

A

central receptors (pons in medulla) become less responsive to stimulus > allows peripheral chemoreceptors of low O2 to take over as stimulus of respiration (hypoxic drive)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

peripheral chemoreceptors

A

located in common carotid artery

low O2

monitor O2 levels, more sensitivity

breathing changes when these receptors take over

“I don’t care if you wanna eat or not”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

central receptors

A

high CO2

“Please eat!!”

In brain - pons and medulla (located near respiratory center in medulla)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

baroreceptors (for BP)

A

located in aortic arch and carotid artery > can send signals to ANS depending on BP > if systolic BP drops > SNS is stimulated to increase HR and RR

ANS = SNS AND PNS

clinical: If BP is going down > HR will go up
- less blood to parts so body compensates to increase HR
- Breath faster to get more O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

dyspnea

A

perceived or feeling of shortness of breath or difficulty breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

cough

A

prevents accumulation of secretions and and entry of irritating substances

defense mechanism of body to get rid of foreign substances in resp tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

cough expectorants

A

mucolytics, liquify secretions

use for AMs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

cough suppressants

A

reduce cough

use for sleep or when infection not present

ex: lecturing > talking > take cough suppressants to solve (bc prob not due to infection)

23
Q

hemoptysis

A

from lungs, coughing up sputum that contains blood

24
Q

hematemesis

A

from GI, blood in vomit

25
Q

atelectasis

A

collapse of alveoli

expose to pneumonia and affects perfusion

26
Q

hypoxia

A

insufficient O2 levels

dead space and shunting can lead to hypoxia

27
Q

pneumonia

A

inflammation of lung tissues

28
Q

cap

A
  • Used to describe infections from organisms found in the community rather than in the hospital or nursing home
  • Infections that begins outside the hospital or is diagnosed within 48 hours after hospital admission to as person who has NOT resided in a long-term care facility for 14 days or more before admission
  • Had prior entering hospital, dx within first 48hrs > covers hospital so cannot be blamed
  • Most common CA = streptococcus pneumoniae
29
Q

hap

A

hospital acquired pneumonia

  • Pneumonia that was not present or was not incubating on admission to the hospital (occurring 48 hrs or more after admission)
  • VAP - special type of HAP
  • Most common cause = staphylococcus aureus particularly MRSA (methicillin-resistant SA)
  • For VAP, in addition to MRSA, enterococcus is common like VRE (vancomycin-resistant enterococcus)
30
Q

vap

A

ventilator associated pneumonia

31
Q

pneumonia in immunocompromised person

A

common causes = s. aureus, aspergillus, candida

fungal related

32
Q

aspiration pneumonia

A
  • Accidental inhalation of substances
  • Poor swallowing
  • Reflux from stomach contents
  • Comatose
  • Must have patients in an elevated head position to reduce reflux (Cannot have patients fully supine = dangerous esp for older)
  • Will be placed on special diet > speech consult (Recommend = thicken liquids, thin is harder to swallow)
33
Q

typical pneumonia

A

bacterial pneumonia

cap, more inflammation and inflammatory response

34
Q

atypical pneumonia

A

viral or nonbacterial penumonia

viral has less striking symptoms, more dangerous

35
Q

pneumonia etiology

A
  • Most common are bacteria and viruses
  • Inhalation of chemicals
  • Aspiration of oropharynx contents
  • Accidentally inhales (saliva, mucous, etc)
  • Infectious agents like fungi
36
Q

pneumonia and flu

A

major risk factor

can alter pulmonary immune defenses (eventually lowering the resistance) > secondary pneumonia

37
Q

pneumonia pathophysiology

A

cause > enters upper airways (inhale and reaches nose, pharynx, larynx) > reaches lungs and other parts of resp tract > CA adheres to respiratory epithelial cells (worse if a lot of secretions are there bc secretions are a good medium for CA/sticks well)&raquo_space;>

  1. Stimulates inflammatory resp&raquo_space; s/s of inflammation
  2. Resp cells try to produce mucous = attempt to counteract microorganisms in the hope that when you cough, you cough out the microorganism
  3. Resp cells are irritated by foreign substance&raquo_space; cough

Mucus plus effect of inflammatory response > exudative fluids > accumulation in alveoli > crackles through stethoscope > alveoli are downed with secretions > SOB and s/s of hypoxia

38
Q

restrictive and obstructive lung disorders

A

caused by conditions that limit expiratory airflow

ex: asthma, COPD, bronchiectasis

restrictive lung disorders are characterized by reduced lung expansion (lungs don’t expand properly)

ex: pulmonary fibrosis, thoracic cage deformities (kyphosis - quasimodo)

39
Q

restrictive and obstructive lung disorders: hypercapnia causes

A

increase CO2 in blood

  • PCO2 > 45 mmHg
  • Usual cause = bradypnea (slow breathing)
  • Other causes = asphyxiation, aspiration, pneumonia, pulmonary edema
40
Q

chronic hypoxia

A

like hypoxemia = diminished level of O2 in the blood

41
Q

COPD

A

chronic obstructive pulmonary disease

COPD related to chronic bronchitis, emphysema, chronic asthma

42
Q

major cause of COPD

A

smoking

other genetic predisposition, IV drug users (develop comorbidity to lead to COPD), exposure to occupation dusts and chemicals

low level of O2

(remember - normally it is the increased level of CO2 that stimulates one to breathe)

CO2 levels is chronically high so it is LOW LEVEL OF O2 THAT STIMULATES

43
Q

COPD manifestations (3)

A
  1. Absent during the early phase
  2. Dyspnea = usually first symptom
    - Can easily be ignored (“I’m just tired”)
  3. Cough or wheezing
    - No respiratory infection but keep coughing = sign for COPD
44
Q

COPD and chronic CO2

A
  • CO2 chronically elevated so peripheral chemoreceptors take over to breath
  • Give more O2 > remove hypoxic drive > cannot breath on own > sleepy or coma
  • Worry about O2 stats?
    a. Cannot breathe = give O2 (goal is to relieve SOB)
    b. No s/s but low O2 state = can wait, depends on display of s/s
45
Q

chronic bronchitis

definition, smoking leads to (2

A

inflammation of the bronchi persisting over a long time

smoking + recurrent respiratory infections > hypersecretion of mucus in large airways >

a) sputum over production
b) affectation of small airways (bronchioles)

46
Q

chronic bronchitis and affectation of small airways (2)

A

affectation of small airways > increased mucus production > plugging of the airways > hypoxia >

a) cyanosis > “blue bloater”
- Cyanosis + generalized edema = “blue bloater”
b) stimulation of pulmonary arterial vasoconstriction

47
Q

chronic bronchitis and stimulation of pulmonary arterial vasoconstriction

A

stimulation of pulmonary arterial vasoconstriction > increased resistance to pulmonary artery > affectation of the right ventricle > right ventricle hypertrophy

> > affectation of right atrium, then superior vena cava and inferior vena cava > congestion, edema > right ventricular heart failure (cor pulmonale)

48
Q

pulmonary hypertension

A

increase pressure of pulmonary artery > affects R ventricle (hypertrophy) > back up of blood into R atrium > back up into SVC (traffic jam)

can be caused by chronic hypoxia

49
Q

cor pulmonae

A

R ventricular failure due to pulmonary HTN there before chronic bronchitis/noncardiac heart failure (failure is in lungs)

50
Q

emphysema

A

a condition in which the air sacs of the lungs are damaged and enlarged, causing breathlessness
Cause: smoking and inherited deficiency of alpha1-antitrypsin (makes lungs prone to injury)

51
Q

alpha1-antitrypsin

A

anti protease enzyme, protects lungs from injury

52
Q

emphysema and smoking

A

smoking >

a) attraction of inflammatory cells (cells in long) > release of elastase
- Normally alpha 1 antitrypsin prevent the release of elastase
b) diminishes α 1 antitrypsin activity (antitrypsin inhibits the release of elastase)

end result

elastase > destroys elastic fibers in the lungs > loss of lung elasticity (recoil) > alveoli become hyperinflated (permanently) > remain oxygenated (early stages) > person appears pinkish (bc more O2) > “pink puffer” (purse lip puffing)

53
Q

hyperinflated alveoli

A

eventually they will burst/rupture and form air pocket (trapped) and can no longer complete exchange of gases

54
Q

late stage of emphysema

A

patient may/can eventually develop cyanosis

Path Exam 1 (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions