Brainscape's Knowledge GenomeTM

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


See full index

x 6102 Pathophys > resp > Flashcards

resp Flashcards

1
Q

dorsal respiratory group

A

set rhythm: resp

send impulses to resp muscles

receive info from carotids + aortic bodies re: PaO2/PaCO2

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

ventral respiratory group

A

stimulated when extra resp effort needed, otherwise dormant

fight or flight = kick in to give extra resp drive

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

apneustic + pneumotaxic centers

A

in pons - modifies breathing pattern

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

normal respiratory quotient

A

aka ventilation-perfusion ratio

0.8

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

Henry’s Law

A

the amount of O2 dissolved in blood = proportional to partial pressure of O2 in blood

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

acute respiratory failure: type 1

A

hypoxemic
PaO2 lt 50mmHg

  • hypoventilation
  • diffusion limitation
  • shunt
  • V/Q mismatch
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

acute respiratory failure: type 2

A

hypercarbic

PCO2 gt/eq 50 mmHg

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

diffusion limitation

A

relates to Type 1 respiratory failure

PaO2 lt PAO2

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

right to left shunt

A

passage of blood from pulmonary to systemic circulation without encountering alveolar gases

ex: atelectasis, pneumonia (alveoli not fully ventilated)
ex: congenital heart defect involving venous mix with arterial (PDA, Tetralogy)

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

VQ mismatch

A

relates to Type 1 respiratory failure

ventilation or perfusion issue

4x

  • normal
  • low V/Q
  • shunt (very low) V/Q
  • high V/Q
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

low V/Q

A

impaired ventilation

ex: hypoventilation post surgery

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

shunt V/Q

A

blocked ventilation (collapsed alveolus)

ex: pneumonia, atelectasis

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

high V/Q

A

low perfusion

ex: PE

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

transudative pleural effusion

A

thinner viscosity, almost consistency of water
- fluid out of capillaries d/t increased intravascular hydrostatic pressure

ex: heart failure

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

exudative pleural effusion

A

thicker, more mucoid; contains WBC and plasma
- capillary beds are diseased + increased permeability = leak

indicative of malignancies, infectious et, inflammatory response

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

empyema

A

pleural effusion that develops an infection that is purulent

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

1 reason for patient post op to have decreased O2 sats

A

atelectasis

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

common in post-surgical and trauma due to pain

A

atelectasis

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

compression atelectasis

A

external pressure on lung

ex: tumor, ascites, profound abdominal distension

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

absorption atelectasis

A

inhalation of high concentrations of O2

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

surfactant impairment

A

can lead to atelectasis

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

atelectasis types x3

A

compression
absorption
surfactant impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

pulmonary edema

A

excess water in lung
- lost balance between capillary hydrostatic and oncotic pressures

most common cause: L sided heart failure

24
Q

ARDS: exudative (inflammatory)

A

first 72 hours

damage: alveolocapillary membrane

activation: inflammatory response
- neutrophils release proteolytic enzyme/free radicals = exacerbation

25
Q

ARDS: proliferative

A

4-21 days

intraalveolar hemorrhagic exudate = more granular = MORE HYPOXEMIA

26
Q

ARDS: fibrotic

A

14-21 days

remodeling & fibrosis

  • fibrosis damages alveoli & respiratory bronchioles
  • gas exchange impaired

PERPETUAL SEVERE R-L SHUNT

27
Q

obstructive pulmonary disease x3

A

asthma
chronic bronchitis
emphysema

28
Q

asthma

A

obstructive pulmonary disease

affects bronchial mucosa: mucus, edema, rigid muscles

  • bronchial hyperresponsiveness
  • airway constriction
  • airway obstruction (variable, reversible)
29
Q

asthma patho

A

early:
1. antigen exposure (activates dendritic cells) = cytokines released

  1. eosinophils cause direct tissue injury via toxic substances (exacerbate hyperresponse)
  2. neutrophils = more inflam
  3. outcome: increased cap perm, mucosal edema, bronchospasm, copious mucus
late:
airway remodeling (permanent damage)
30
Q

COPD

A

obstructive pulmonary disease

  1. chronic bronchitis
  2. emphysema

in central airways, small peripheral airways, and lung parenchyma

3rd cause of death in US

PREVENTABLE

31
Q

COPD risk factors x4

A

smoking (95%)

occupational exposures

environmental

genetic (alpha-1 antitrypsin small)

32
Q

chronic bronchitis

A

obstructive pulmonary disease; form of COPD

airway inflam d/t neuts, macs, lymphocytes

2. inflam results: bronchial edema, increased mucus glands/goblet cells = copious mucus
\++ impaired cilia = hard to clear = persistent, productive cough
  1. from larger bronchi eventually to affecting airways diffusely
33
Q

emphysema

A

obstructive lung disease, form of COPD

permanently enlarged acini

destruction alveolar walls

primary: a1 antitrypsin (small %)
secondary: inhalation related

34
Q

primary emphysema

A

less common, a1-antitrypsin

35
Q

acinus (acini)

A

respiratory bronchioles

alveolar duct

alveolar sacs (alveoli)

36
Q

secondary emphysema

A

more common, inhalation related

37
Q

emphysema patho

A
  • alveoli destruction d/t elastase release: BREAKDOWN/DAMAGE OF ALVEOLAR WALL
  • cellular apoptosis =
    1. loss of alveoli
    2. decreased surface area for gas exchange
  • bullae/blebs = can rupture, bleed
  • airtrapping + loss of elastic recoil (OBSTRUCTIVE)
38
Q

most common cause of pneumonia

A

aspiration

39
Q

pneumonia + patho

A

infection of lower respiratory tract

alveolar macrophages: first responders

neutrophils: aid in phago + neutrophil extracellular trap (NET) - catch bact for efficient destruction

40
Q

most common type of pneumonia

A

community-acquired pneumonia

41
Q

tuberculosis cause & route

A

mycobacterium tuberculosis

airborne droplets

42
Q

tuberculosis patho

A

survive in macrophages, resist lysosomal killing

43
Q

Virchow’s Triad

A

venous stasis
hypercoagulability
endothelial damage

PULMONARY EMBOLISM RISK FACTORS

44
Q

pulmonary embolism + common findings

A

partial/full occlusion pulmonary artery

pleuritic chest pain (+/-)
dyspnea
tachypnea
tachycardia
decreased O2 sat

PE usually s/t other probs, detected via other means (ABG, hypoxic, etc)

45
Q

pulmonary artery hypertension

A

d/t narrowing of arteries carrying blood from heart to lungs

if progresses for too long can develop into right heart failure

46
Q

mean pulmonary artery pressure normal vs pulmonary artery hypertension

A

normal 15 - 18

pulm art htn gt 25

47
Q

most common cause of pulmonary artery hypertension

A

COPD

idiopathic (rare), familial possible too

48
Q

leading cause of cancer deaths in the US (men + women)

A

lung cancer

49
Q

most common cause of lung cancer

A

tobacco smoking

50
Q

pulmonary artery vasoconstriction reasons x3

A

acidemia

hypoxic pulmonary vasoconstriction

low PAO2

51
Q

Fick’s Law

A

volume gas moving across tissue sheet proportional to

  • sheet area
  • diffusion constant
  • different in partial pressure

FICK AIN’T THICK

52
Q

minute ventilation equation

+ normal

A

MV = RR x TV

normal: 6-10 L/min

53
Q

lung receptors x3

A

irritant

stretch

J-receptors

54
Q

irritant lung receptors where & action & triggers

A

conducting airway epithelium

cough

aerosols, gases, particulates

55
Q

stretch lung receptors where & action

A

airway smooth muscle

decrease lung rate/vol to prevent injury

56
Q

J-receptor lung receptors where & triggers & action

A

near capillaries in alveolar septa

respond to increased capillary pressure

rapid shallow breathing, laryngeal constriction, mucus secretion, hypotension, bradycardia

x 6102 Pathophys (6 decks)

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