Brainscape's Knowledge GenomeTM

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


See full index

BSNC 5000 > Module 3 - Gas exchange & immunity > Flashcards

Module 3 - Gas exchange & immunity Flashcards

1
Q

When do Type 2 alveolar cells begin to produce surfactant?

A

~28-30 weeks gestation

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

What are the 4 types of hypersensitivity

A

Type 1 - IgE mediated allergies
Type 2 - IgM/IgG auto antibodies
Type 3 - antibody complexes
Type 4 - T-cell mediated –> macrophages/cytotoxic T-cells

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

What is bronchiolitis

A

acute lower respiratory tract infection
targets lung EPITHELIUM (not affected by bronchodilators)

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

Which virus typically causes bronchiolitis?

A

respiratory synctycial virus
other viruses: parainfluenza, mycoplasma, adenovirus

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

What age is bronchiolitis most common?

A

<2 years old

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

Respiratory anatomy of infants/children

A

narrow airway (funnel shaped, anterior facing)
narrowest part = cricoid making intubation difficult
immature intercostal muscles –> diaphragm primary mode of breathing
horizontal intercostal muscles –> rib cage moves up/down vs. up/out
abdominal breathing
obligate nose breathing until 6 months
shorter airway –> higher risk of lower respiratory infections
narrower lumen –> higher risk of obstruction

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

Types of retractions

A

tracheal tug
substernal
suprasternal
supraclavicular
intercostal
subcostal

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

Infant ventilation

A

extrathoracic airway narrow during inspiration and widen during expiration
inthrathoracic airway widens on inhalation and narrows on expiratoin
asymmetrical movement helps move air towards lungs

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

Extrathoracic definition

A

trachea

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

Intrathoracic

A

below trachea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Functional residual capacity

A

volume remaining in lungs after exhalation

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

Infant sleep & breathing

A

reduced gas exchange
reduced muscle tone –> narrower airway
shorter exhalations = increased functional residual capacity (reduced G/E)r
reduced intercostal activity

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

Intermittent breathing

A

normal for infants to stop breathing for up to 15 seconds

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

True infant apnea

A

no breathing for >20 seconds

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

Restrictive lung disorders

A

pulmonary edema
respiratory distress syndroem

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

Obstructive lung disorders

A

asthma
allergies?

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

Croup sounds

A

stridor on inspiration

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

Asthma sounds

A

prolonged expiration, wheezing

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

Cortisol and surfactant

A

increase maturation of Type 2 alveolar cells & increase surfactant production

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

Insulin and surfactant

A

decrease production fo surfactant

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

URTI

A

inflammation of upper airway –> impacts inspiration

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

LRTI

A

inflammation of lower airways –> impacts expiration
*air trapping, prolonged expiration

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

URT anatomy

A

nose
mouth
sinuses
larynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

LRT anatomy

A

trachea
bronchi
bronchioles -> alveoli
lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

S/S impending respiratory failure

A

increased WOB
retractions
grunting
reduced chest movement
cyanosis not relieved by O2 therapy
HR >150 OR increasing/decreasing bradycardia
tachypnea or bradypnea
extreme anxiety/agitation
fatigue
reduced LOC

26
Q

Bronchiolitis Treatment

A

1)O2 therapy (humidifed)
2)hydration (IV, NG)

other:
positioning (elevate head)
reduce fatigue
nasal suction (infants)
epinephrine/dexamethasone

27
Q

Syncytia

A

merging of epithelial cells d/t RSV

28
Q

CD8 T-cells

A

differentiate into cytotoxic T-cells

29
Q

CD4 T-helper cells

A

TH1 –> stimulate cytotoxic T-cells
TH2 –> stimulate B-cells to differentiate into plasma cells. Promote class switching

30
Q

Which T-helper cell is more commonly associated to allergies?

A

TH2
*TH2 shift occurs in pregnancy –> more prone to developing allergies

31
Q

Mechanism of TH1 hypersensitivity

A

APC presents antigen to TH2 –> TH2 cells rls mediators that cause B-cells to differentiate into IgE producing cells
IgE antibodies bind to allergen
IgE antibodies bind to mast cells via Fc region –> PRIMING
on secondary exposure, allergen crosslinks IgE antibodies on mast cell surface cause mast cell degranulation –> allergic symptoms

32
Q

Where are mast cells located?

A

connective tissue
skin
mucous membranes
adjacent to blood/lymph vessels

33
Q

Where are basophils located?

A

bloodstream

34
Q

Type 1 phases

A

Primary/immediate –> mast cells
Secondary/late –> inflammatory cells sustain inflammation

35
Q

Mechanism of Type 2 hypersensitivity

A

IgG or IgM antibodies target endogenous/exogenous antigens located on cell surface
1) complement/antibody mediated cell destuction
2) “ inflammation
3) antibody-mediated cellular dysfunction

36
Q

Mechanism of Type 2 hypersensitivity

A

IgG or IgM antibodies target endogenous/exogenous antigens located on cell surface
1) complement/antibody mediated cell destuction
2) “ inflammation
3) antibody-mediated cellular dysfunction

37
Q

Types of T2 hypersensitivity reactions

A

blood transfusion reactions
hemolytic disease of newborn

38
Q

Virus components

A

genetic material –> DNA or RNA
protein capsid
envelope (cell membrane attached to virus –> OPTIONAL)

39
Q

What type of virus evolves more rapidly?

A

RNA

40
Q

Bronchiolitis patho

A

epithelial inflammation
pulmonary edema
increased mucus production —> mucus plug
tissue necrosis

41
Q

What is asthma?

A

chronic obstructive respiratory disease that causes airway inflammation, edema, mucus production and bronchospasm

42
Q

Common asthma triggers in children

A

viral RTI
allergens
air pollution
seasonal changes
reduced medication compliance

43
Q

PRAM

A

pediatric respiratory assessment measure

44
Q

Asthma treatment

A

bronchodilators
anticholinergics
systemic corticosteroids
O2 therapy
magnesium sulfate (relax smooth muscle)
IV drugs
intubation/ventilation
Bipap/CPAP

45
Q

Asthma & breathing

A

a lack of wheezing/silent chest can indicate the airway was completely closed and respiratory failure is imminent

46
Q

PRAM scores

A

mild 0-3
moderate 4-7
severe 8-12

47
Q

Asthma symptoms

A

1) dyspnea, chest tightness, wheezing, sputum production, and cough,
2) airflow obstruction (s/t inflammation)
3) bronchial hyperresponsiveness (IgE mast cells)
4) underlying airway inflammation

48
Q

Types of asthma

A

atopic
non-atopic

49
Q

Atopic asthma

A

type 1 hypersensitivity reaction
caused by IgE antibodies responding to allergens

50
Q

Non-atopic asthma

A

non-allergenic asthma. caused by triggers such as viral infection, stress, pollution, exercise, etc.

51
Q

Systemic effects of corticosteroids

A

adrenal suppression
growth impairment
decreased bone density
myopathy
weight gain

52
Q

Layers of respiratory tract

A

mucosa (epithelium + lamina propria)
submucosa
basement membrane
cartilage/smooth muscle/adventitia

53
Q

How does aspirin promote asthma?

A

aspirin = nsaid
inhibition of COX pathway leads to increased LOX activation
increased LOX = increased immune response –> hyperreactivity

54
Q

Long-term effects of asthma

A

smooth muscle & goblet cell hypertrophy
injury to epithelium
blood vessel proliferation

55
Q

Asthma phases

A

Early phase 10-20 onset caused by IgE antibodies
Late phase 4-8 hrs post exposure -> inflammatory cells rls mediators prolonging inflammation

56
Q

Leukotrienes & inflammation

A

bronchoconstriction
increased bronchial reactivity
mucosal edema
mucous hypersecretion

57
Q

How do infants breath

A

extrathoracic airway narrows on inspiration, widens on expiration
intrathoracic airway widens on inhalation, narrows on expiration

58
Q

Incubation of RSV

A

2-8 days

59
Q

Stages of extrinsic asthma

A

1) sensitization
2) provocation

60
Q

Phases of an asthma attack

A

early (within minutes d/t IgE antibodies)
late (hours d/t rls of inflammatory cells/mediators)

BSNC 5000 (11 decks)

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