Brainscape's Knowledge GenomeTM

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


See full index

patho > respiratory disorder > Flashcards

respiratory disorder Flashcards

1
Q

rhinorrhea upper/lower

A

upper

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

cause of rhinorrhea

A

increased production of mucus> congestion
increased secretion from lacrimal glands draining into the nasal cavity
exposure to cold air

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

rhinitis upper/lower

A

upper

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

rhinitis

A

inflammation of nasal mucosa spreads from nose to throat to chest

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

rhinitis results

A

sinusitis
via spreading inflammation to tear ducts and paranasal sinuses, causing blockage of sinus passageway

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

types of rhinitis

A

allergic and non allergic

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

non allergic rhinitis caused by

A

air pollution, smoke, strong odor

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

explain allergic rhinitis reaction
ex. pollen

A

pollen binds to the b receptor> b cell differentiate into plasma cell>plasma cells make IgE antibodies> attaches to mast cell and basophils via the constant region of IgE antibody
When 2nd exposure, IgE binds tothe variable region of pollen> degranulation of mass cell>release of histamine & inflammatory mediators> congestion&leakiness of capilaries

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

sinus infection caused by

A

germs growing in the accumulated mucous

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

sinus headaches caused by

A

pressure change

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

3 types of lung receptor

A

stretch receptors, irritant receptors, juxtacapillary receptors

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

stretch receptors located at

A

smooth muscle layer

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

stretch receptors responds to

A

changes in pressure in airway

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

irritant receptor located at

A

between airway and epithelial cells

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

irritant receptor respond to

A

noxious gases, dust, cold air

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

juxtacapillary receptors located at

A

alveolar wall

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

juxtacapillary receptor senses

A

congestion

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

cough reflex

A

primary defense mech for respiratory syst

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

cough reflex receptors located at

A

throat and trachebronchial wall

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

cough reflex process

A

vagus nerve transmits signal to the medulla > leads to rapid large inspiration of air, forceful contraction of abdominal and expiratory muscle

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

2 general cause of respiratory dysfunction during spirometry

A

restrictive lung disease, obstructive lung disease

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

restrictive lung disease

A

decrease in total lung capacity from structural or functional lung changes
difficulty expanding lungs

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

obstructive lung disease

A

increase in airway resistance

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

restrictive lung disease causes TLC and forced expiration to

A

decrease
> 80% FEV1/FVC ratio

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

restrictive lung disease examples

A

pulmonary fibrosis, sarcoidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

pulmonary fibrosis

A

accumulation of fibrous tissues in the lungs when alveoli are damaged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

cause of pulmonary fibrosis

A

inhalation of small particles
(fine needles)
the problem gets bigger when try to remove them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

lung tissue, vital capacity, forced expiration in obstructive lung disease

A

lung tissue, vital capacity normal, forced expiration reduced
FEV1/FVC <70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

obstructive lung disease example

A

asthma, bronchiectasis, bronchitis, COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

4 other conditions affecting respiratory function

A
  1. diseases affecting diffusion of O2 and CO2
  2. reduced ventilation due to mechanical failure
  3. failure of adequate pulmonary blood flow
  4. V/Q abnormalities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Edema

A

thickening of the respiratory membrane leading to inadequate gas exchange and oxygen deprivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

emphysema

A

decrease in surface area due to thickening of respiratory membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

obstructive sleep apnea

A

chronic disorder of intermittent cessation of breathing during sleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

cause of obstructive sleep apnea

A

partial/complete collapse of the UPPER airway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

risk factor of obstructive sleep apnea

A

age, male, obesity, cranio facial and upper airway abnormalities, nasal congestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

symptoms of obstructive sleep apnea

A

snoring, fatigue, restless sleep, awakening with chocking and gasp, nightmare, changes in mood, cognitive deficits, headache, GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

obstructive sleep apnea treatment

A

wt loss, continuous positive airway pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

developmental lung disorder and infection in children

A

sudden infant death syndrome, neonatal respiratory distress syndrome, bronchiolitis, croup

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

sudden infant death syndrome

A

etiology unknown, happens to infant under one

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

neonatal respiratory distress syndrome

A

alveolar collapse due to decreased surfactant in premature babies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

process of neonatal respiratory distress syndrome

A

decreased surfactant & immature lung structure > decreased lung compliance>atelectasis (airway collaspe)>hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

hypoxia can lead to

A
  1. pulmonary vascular constriction > pulmonary hypertension>decreased pulmonary perfusion
  2. increased pulmonary capillary permeability>movement of capillary fluid into alveoli>hyaline membrane formation > shedding of dead cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

neonatal respiratory distress syndrome symptoms

A

cyanosis, flaring nostrils, tachypnea, tachycardia, grunting sounds with breathing, poor feeding, chest retractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

bronchiolitis

A

bronchioles swell and get congested

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

cause of bronchiolitis

A

respiratory syncytial virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

symptom of bronchiolitis

A

cyanosis, wheezing, intercostal retraction, fever (bc it’s a infection), coughm tachypnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

croup

A

inflammation of the larynx and subglottic airway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

cause of croup

A

viral URI (parainfluenza virus type 1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

hallmark sign of croup

A

barking cough, stridor on inspiration/expiration,fever,drooling, tachypnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

croup occurs at

A

trachea causing epiglottis to narrow (“steeple sign”)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

treatment of croup

A

depends on severity
oral hydration, calming down, moist air
drugs: steroids(dexamethasone), epinephrine
intubation when serious

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

infection of respiratory system

A

acute respiratory distress syndrome, corona virus, bronchitis, pneumonia, tuberculosis, ghon complex,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

acute respiratory distress syndrome

A

acute abnormalities of both lungs, rapidly progressing inflammatory lung injury: pro-inflammatory cytokines, increased pulmonary permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

acute respiratory distress syndrome cause

A

due to septic shock, penumonia, aspiration of gastric content, vomit, overdose of ASA/cocaine/opioids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

acute respiratory distress syndrome leads to

A

diffuse alveolar damage, hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

symptoms of acute respiratory distress syndrome

A

cyanosis, dyspnea, flaring nostrils, tachypnea, tachycardia, diaphoresis, use of accessory respiratory muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

progression of corona virus (severe acute respiratory syndrome)

A

SARS-CoV>MERS-CoV>SARS-CoV-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

SARS-CoV-2

A

single stranded positive sense RNA virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

entry receptor of SARS-CoV-2 and why does that matter

A

ACE2 receptor, it has widespread distribution: vascular endothelial cells, oral and nasal mucosa and nasopharynx, kidneys, cardiac myocytes, lungs including alveolar epithelial cells, GIT including small intestine and the liver, brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

T/F
Covid is not just a respiratory virus bc it attaches to anything that has ACE 2 recpetor

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

effect of covid 19

A

direct cytotoxic effect
when meet cell, dead

62
Q

covid virus binding with ACE 2 receptor with TMPRSS2 leads to (RAAS system)

A

ACE2 receptor breaking down angiotensin 2 > increased angiotensin 1-7> binds to Mas-R>vasodilation

63
Q

TMPRSS2

A

modifies spike protein so covid virus binds better with the ACE receptor

64
Q

decrease number of ACE 2 receptor leads to

A

vasoconstriction

65
Q

inflammatory pathway of covid virus

A

shedding ACE2 receptor from the cell surface

66
Q

thromboinflammation of covid virus

A

virus+endothelial cell > activate factor 3, decrease fibrinolysis, increase thrombin production >formation of clot> Q(perfusion) decrease

67
Q

dysregulated immune response of covid virus

A

neutrophil causes
1. NET(neutrophil extracellular trap)> histone +free DNA> activate instrinsic pathway>coagulation
2. ROS> inactivate surfactant> risk of alveoli collaspe increas, shedding of alvoli type 1 cell, leukotriene&MMP activated &release > destruction of alveoli

68
Q

sign of severe Covid

A

lung ground glass opacities and consolidation on chest X-ray or CT
drop in PO2
increased levels of IL-6
increased C-reactive protein levels and erythrocyte sedimentation rate
elevated fibrinogen and d-dimer levels
development of a cytokine storm

69
Q

consequences of severe covid

A

pneumonia, sepsis, lung damage, heart damage, coagulation abnormalities: sepsis-induced coagulopathy, microvascular thrombosis, macrovascular arterial and venous thrombosis

70
Q

mechanism of coagulation abnormalities

A

complement activation, NET components of cell-free DNA and histones activate the intrinsic pathway of coagulation , inhibition of fibrinolysis by increasing the activity of PAI-1, damage of endothelial cells leads to inflammation, apoptosis, release of tissue factor and platelet aggreagation

71
Q

post covid syndrome also called

A

long haulers

72
Q

multisystem inflammatory syndrome in associated with covid

A

mostly child, symptoms develop after the infection, can lead to chock and multiple organ failure, similar to Kawasaki disease,
interferon doesn’t do its job and interleukins level increase

73
Q

bronchitis

A

inflammation of lining of bronchi

74
Q

cause of acute bronchitis

A

virus causing URI, bacteria

75
Q

symptoms of bronchitis

A

cough, production cough, SOB, chest tightness

76
Q

pneumonia

A

inflammation of lung parenchyma including alveoli and bronchioles, fluid accumulation in the alveoli

77
Q

cause of community-acquired pneumonia

A

bacteria (pneumococcus/mycoplasma)

78
Q

lobar

A

affects an entire lobe of the lung

79
Q

bronchopneumonia

A

patchy distribution over more than one lobe

80
Q

atypical pneumonia

A

viral and mycoplasma infections of the alveolar septum or interstitium (중요, typically inside the lumen not interstitium)

81
Q

nosocomial pneumonia

A

병원 드러버서 걸린 거

82
Q

cause of tuberculosis

A

mycobacterium tuberculosis hominis

83
Q

mycobacterium tuberculosis hominis

A

aerobic, protective waxy capsule, spread by droplets from respiratory secretion of infected pts, can stay alive in “suspended animation” for yrs

84
Q

initial tb infection

A

macrophages begin a cell-mediated immune response, resulting in a granulomatous lesion/ghon focus containing: macrophages, t cells, inactive tb bacteria > activate cell mediated T cell > delayed type 4 immune response

85
Q

secondary tb infection

A

reinfection or reactivated tb > progressive or disseminated tb

86
Q

ghon complex

A

nodules in lung tissue and lymph nodes, caseous necrosis, calcium may deposit in the fatty area of necrosis, visible on x-rays

87
Q

tb vaccine

A

if you take a PPD test, the result is always positive

88
Q

latent tb infection

A

no symptoms, but positive on the test, should consider treatment for latent TB infection to prevent TB disease

89
Q

disorder of the pleura

A

pneumothorax, pleural effusion

90
Q

pneumothorax (lung collapse)

A

caused by equalization of the intrapleural pressure with the intrapulmonary pressure > transpulmonary pressure keeps the airways open

91
Q

pneumothorax leads to

A

trauma, infection (TB, pneumonia), lung cancer

92
Q

symptoms of pneumothorax

A

sudden chest pain, sob

93
Q

risk factor for pneumothorax

A

males, pre-existing lung disease, smoking, FH or prior history, mechanical ventilation

94
Q

types of pneumothorax

A

tension, open

95
Q

tension pneumothorax

A

air enters pleural cavity through wound on inhalation, cannot leave on exhalation
들어올 순 있는데 나갈 수가 없음
more severe

96
Q

open pneumothorax

A

air enters pleural cavity through the wound on inhalation and leaves on exhalation
너무 자유롭게 들낙

97
Q

pleural effusion

A

fluid in the pleural cavity

98
Q

pleural effusion includes

A

hydrothorax, empyema, hemothorax

99
Q

Hydrothorax

A

serous fluid occur with inflammatory condition ex. inflammatory disease

100
Q

Empyema

A

pus, caused by bacterial infection, need antibiotics

101
Q

Hemothorax

A

blood, caused by trauma/cancer

102
Q

bronchial obstructive disorders

A

atelectasis, asthma, copd, emphysema, chronic bronchitis

103
Q

atelectasis

A

incomplete expansion of a lung or portion of the lung

104
Q

cause of atelectasis

A

bronchial obstruction: mucus, foreign object, tumor, enlarged lymph node

105
Q

asthma

A

chronic inflammatory disorder of the airways

106
Q

asthma characterized by

A

recurring symptoms of reversible airway obstruction, bronchial hyperresponsiveness and bronchospasm, increased mucus secretions and release of inflammatory mediators

107
Q

treatment for asthma

A

beta2 agonist bronchodilator (albuterol) to reduce symptoms
but need to take care of the inflammation

108
Q

atopy

A

genetic predisposition for the development of IgE-mediated response to allergens, strongest predisposing factor for asthma development

109
Q

adult onset asthma

A

atopy, family history, occupational exposure to chemicals, viral infections, cig, environmental pollution, premature birth

110
Q

inflammatory cells/mediators involved with asthma

A

neutrophils, lymphocytes, mast cells, macrophages, eosinophil recruitment

111
Q

neutrophil w/ asthma

A

severe sudden onset fatal asthma, occupational asthma, in smokers

112
Q

lymphocytes ( T helper cell) w/ asthma

A

release cytokines that modulate eosinophil adherence, migration, and activation

113
Q

Mast cell w/ asthma

A

IgE-mediated release of histamine and leukotrienes> airway remodeling: irreversible changes that result through chronic yrs of inflammation

114
Q

Macrophages w/ asthma

A

release of inflammatory mediators like leukotrienes

115
Q

eosinophil recruitment w/ asthma

A

causes epithelial cell damage, mucus hypersecretion, increased smooth muscle reactivity

116
Q

asthmatic bronchioles

A

lumen clogged up w/ mucus, contraction of the smooth muscle

117
Q

pulmonary function monitoring

A

PRFR: peak expiratory flow rate

118
Q

mild intermittent asthma

A

less than 2x per week
need rescue inhaler

119
Q

mild persistant asthma

A

more than 2x per week but less than one a day, need rescue inhaler

120
Q

moderate persistant asthma

A

need rescue inhaler and ICS

121
Q

severe persistent asthma

A

can’t talk

122
Q

difference between COPD and asthma

A

beta 2 agonist is not used for COPD

123
Q

COPD

A

trouble exhaling, frequent pulmonary infection, mostly caused by smoking, air trapping > can’t properly oxygenate

124
Q

type of COPD

A

emphysema, chronic obstructive bronchitis, bronchiectasis

125
Q

emphysema

A

enlargement of air spaces and destruction of lung tissue
V&Q both affected

126
Q

chronic obstructive bronchitis

A

obstruction of small ariways
only V affected>mismatch

127
Q

bronchiectasis

A

infection and inflammation destroy smooth muscle in airways > permanent dilation, multiple chronic lung infection, hard to exhale

128
Q

general mechanism of COPD

A

inflammation & fibrosis of the bronchial wall
1. hypertrophied mucous glands > productive cough
2. loss of alveolar tissue > decreased surface area for gas exchange
3. loss of elastic lung fibers > airway collapse, obstructed exhalation, air trapping

129
Q

emphysema

A

loss of lung elasticity, enlargement of distal terminal bronchial airways (decreased surface area), destruction of alveoli and capillary beds (V&Q affected) , hyperinflation of lungs (increased TLC), dry cough,

130
Q

emphysema inflammation caused by

A

inhaled irritants, increased infiltration of neutrophils, macrophages, CD8+ T-cells

131
Q

neutrophil w/ emphysema

A

secrete proteases: trypsin & elastase, MMPs (matric metalloproteases) > result in breakdown of elastin and connective tissue

132
Q

alpha- antitrypsin in emphysema

A

inactivates the trypsin before it can damage the alveoli > if don’t have it then alveolar damage

133
Q

chronic bronchitis

A

chronic irritation of airways due to increased number of mucous cells and mucus gland enlargement, mucus hypersecretion, bronchial edema
productive cough
fibrosis and smooth muscle hypertrophy

134
Q

pink puffers

A

emphysema

135
Q

why is emphysema pink puffers

A

increase respiration to maintain oxygen levels, dyspnea, increased ventilatory effort, use accessory muscle
match VQ

136
Q

blue bloaters

A

bronchitis

137
Q

why is bronchitis blue bloaters

A

cannot increase respiration enough to maintain oxygen level, cyanosis and polycythemia, cor pulmonale
VQ mismatch

138
Q

low levels of O2

A

hypoxia

139
Q

high CO2 levels

A

hypercapnia

140
Q

secondary pulmonary hypertension

A

elevation of pulmonary venous pressure, increase pulmonary blood flow, pulmonary vascular obstruction, hypoxemia

141
Q

primary pulmonary hypertension

A

blood vessel walls thicken and constrict

142
Q

cor pulmonale

A

right-sided heart failure secondary to pulmonary disease

143
Q

cor pulmonale leads to

A

decreased lung ventilation, increased workload on the right heart, decreased oxygenation, kidney releases erythropoietin>more RBCs made> polycythemia makes blood more viscous, increased workload on the heart

144
Q

cystic fibrosis

A

recessive disorder in chloride transport proteins

145
Q

cystic fibrosis leads to

A

high conc of NaCl in the sweat, less Na and water in respiratory mucus in pancreatic secretion > mucus is thicker > obstructs airways and obstructs the pancreatic and biliary duct 너무 찐득해서 CFTR channel로 나가질 못함

146
Q

health problems with cystic fibrosis

A

gallstones > gallbladder needs to be removed, can’t digest fats (bc no adipose) and vit ADEK

147
Q

3 types of lung cancer

A

squamous cell carcinoma, adenocarcinoma, small cell carcinoma

148
Q

squamous cell carcinoma

A

centrally located in the lungs, arises in bronchial epithelium, strongly associated with smoking, intraluminal growth pattern, result in obstruction, hemptysis

149
Q

adenocarcinoma originates at

A

peripheral lung area derived from mucus-producing glands (aggressive)

150
Q

small cell carcinoma contains

A

lymphocyte-like cells that originate in the primary bronchi > rapid doubling time
grows in the wall NOT lumen

151
Q

characteristic of small cell carcinoma

A

highly metastatic, starts in central airway and infiltrates submucosa, less likely to cause obstruction than squamous cell carcinoma

patho (3 decks)

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