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STEP1 > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Air way obstruction acid base

A

If severeenough to block breathing or cause respiratory failure, respiratory acidosis

In hyperventilation stage with incomplete blockage, respiratory alkalosis

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2
Q

Renal compensation respiratory acidosis

A

Acute: +1 bicarb per +10 co 2
Chronic - +2 per 10 i

Acute-hours

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3
Q

Renal comp respiratory al kalosis

A

Acute: -2 bicarb per - 10 co 2
Chronic -5 per -10

Acute-hours

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4
Q

Primary ciliary dyskinesia

A

Dyenin- ciliary motor protein
Sinus invertus- organs wrong side
Infertility

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5
Q

Kartagener Syndrome

A

‘PCD type
Sinopulmonary infection- bronchiectasis- sinus invertas

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6
Q

DRG

A

Dorsal respiratory group
Solitary nucleus
Medulla
Normal Inspiration
Afferents(in) _ vagus from aortic body and glossopharyngeal from carotid body
Efferent (out) _ phrenic and intercostal

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7
Q

VRG

A

Ventral respiratory group
Medulla
Labored breathing
Active inhalation and exhalation

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8
Q

Pneumotaxic center

A

Upper pons
Inhibits inspiration

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9
Q

Apneustic center

A

Lower pons
Agonal respirations

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10
Q

Hering- Breuer reflex

A

Stretched lungs inhibit inspiration (stop breathing in once lungs are full)
Diminished from chronic lung dissension in copd → extra inflation

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11
Q

Cheyne - stokes respirations

A

CHF
Alternating fast and slow with intermittent central apnea

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12
Q

Chemoreceptor that detects H ions

A

Carotid body
→ cn 9

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13
Q

L/S ratio

A

Lecithin-Sphingomyelin
Measuresfetal lung maturity
In amniotic fluid
> 2, good
<1.5 bad

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14
Q

Pathological shunt

A

Blood perfusion without ventilation
Eg. where there is thickening of alveolar membrane to point of no diffusion

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15
Q

Carina at which rib

A

2

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16
Q

Minor fissure which rib

A

4

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17
Q

Flat percussion note

A

Plural effusion - blood, pus, serous fluid
Normal dense tissue

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18
Q

Hyperresonant lung

A

Pneumothorax

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19
Q

Bronchoprovocation testing

A

Asthma
20% decrease in FEV1
Methacholine or histamine
Then albuterol to reverse

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20
Q

Mist common agents bacterial sinusitis

A

S pneum, H flu, moraxella

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21
Q

Invasive fungal sinusitis

A

Can cause fatal encephalopathy in ic
Aspergillus, mucorales, fusarium

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22
Q

Oxymetazoline

A

a -adrenergic agonist → local vasoconstriction
Nasal congestion
Rosacea
Other allergic

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23
Q

Pseudoephedrine

A

a - adrenergic → local vasoconstriction
Nasal decongestant
Eustachian tube obstruction

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24
Q

Typical_antibiotics bacterial sinusitis

A

Amoxicillin +/- clavulanate
Tmp/smx
Consider if 7 days no improvement

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25
Q

Allergic rhinitis Tx

A

1-intranasal steroids
2- antihistamines
3-cromolyn

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26
Q

Oral antihistamines 2nd gen

A

Cetirizine
Loratadine
Fexofenadine

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27
Q

Intranasal antihistamines

A

Azelastine
Olopatadine

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28
Q

Cromolyn

A

Prevents mast cell degranulation
Allergies
Intranasal

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29
Q

Dominant cell type allergic rhinitis

A

Mast cells (not eosinophils)

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30
Q

Most common agent pharyngitis

A

Adenovirus

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31
Q

GAS pharyngitis Tx

A

Penicillin
Reduces rheumatic fever incidence but not psgn

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32
Q

Gonorrhea Tx

A

Ceftriaxone

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33
Q

Chlamydia t x

A

Azythromycin - macrolide
Doxy

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34
Q

Tonsillitis agents

A

Adenovirus
Gas
Mono

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35
Q

Epiglottit.is agents

A

H flu type B - vaccine - gram neg coccobacill:
Strep
Staph

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36
Q

Examining epiglottis

A

Don’t in kids-can make it worse
X-ray

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37
Q

Croup

A

Larynx and trachea inflammation
Parainfluenza - most common
Rsv
Adenovirus
Flu virus

Kids <3
Barking cough
“Steeple sign’ X-ray

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38
Q

Severe croup Tx

A

Corticosteroids
Inhaled epinephrine
Heliox
Sometimes intubate

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39
Q

Odynophagia

A

Painful swallowing
Common in pharyngitis

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40
Q

Tonsillitis is u sually which tonsils

A

Palatine
Sometimes pharyngeal aka adenoids

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41
Q

Visual cue bacterial vs viral pharyngitis

A

Tonsillar exudate
Don’t give abx if none but still send cultures

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42
Q

pulmonary capillary wedge pressure

A

approximates pressure in left atrium
normal in ARDS
increased in CHF

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43
Q

histology ARDS

A

hyaline membranes= diffuse endothelial damage

44
Q

criteria ARDS

A

Berlin criteria:
- acute onset 1 wk
- bilateral opacifications on CXR - not explained by effusions, collapse, nodules
- noncardiogenic pulmonary edema - normal PCWP
- PaO2/FiO2 ≤300

45
Q

triggers ARDS

A

= diffuse endothelial damage
most common: sepsis (from cytokines)
others:
- pneumonia
- aspiration
- shock
- trauma
less common:
- pancreatitis (from enzymes in circulation)
- fat emboli
- drug OD
- uremia
- blood transfusion

46
Q

signs ARDS

A

very sick
hours to days of trigger
rapid decompensation

SOB
hypoxemia
diffuse crackles
respiratory acidosis (high pCO2)

high A-a gradient
increased physiologic dead space
V/Q mismatch

47
Q

ventilation ARDS

A

almost always needed

settings:
high PEEP - prevents alveolar collapse
low LTVV (low tidal volume ventilation)

48
Q

transient tachypnea of the newborn

A

term/late pre-term
failure to clear alveolar fluid
over-inflated lungs, interstitial edema, respiratory distress
generally resolves spontaneously with supportive therapy

risk:
- C section/lack of labor
- maternal diabetes

49
Q

newborn respiratory distress syndrome

A

any delivery stage
generally lack of surfactant

risk:
- prematurity
- multifetal pregnancies
- maternal diabetes
- genetic mutations surfactant

50
Q

vasodilation after birth

A

O2 –> vasodilation in lungs
alveolar collapse –> no vasodilation, further impedes gas exchange

51
Q

grunting newborn

A

always dt respiratory distress
partial glottal closing
compensatory: increases airway pressure, stents airways, increases functional residual capacity

impending respiratory failure

52
Q

NRDS X-ray

A

ground glass opacities

53
Q

NRDS tx

A

antenatal dexamethasone
exogenous surfactant (direct to lung via brief intubation)
CPAP
O2
severe: inhaled NO (decreases pulmonary vascular resistance)

54
Q

FEV1/FVC normal and path

A

normal = 80%
obstructive < 70%
restrictive = normal to high dt low TLC; FEV1 and FVC both decreased (FEV1 ≥ FVC)

55
Q

PV loop normal and path

A
56
Q

alpha-1-antitrypsin deficiency

A

emphysema
dt failure to destroy destructive elastases
young onset, usually few risk fx, usually family hx

57
Q

bronchiectasis

A

bronchial necrosis and inflammation
dilation and dysfunction
abnormal mucous clearance
e.g. CF

58
Q

pneumoconiosis

A

fibrosis d/t foreign body scarring
e.g. asbestos, coal dust, silica (sand)

59
Q

drug induced ILD

A

amiodarone (antiarrythmetic)
busulfan (alkylating chemo; CML, HSCT)
bleomycin (antitumor antibiotic)

60
Q

extrinsic causes RLD

A

ascites
scoliosis/kyphosis
other scmpression of thoracic space

61
Q

digital clubbing

A

often associated with hypoxemia, restrictive lung disease

62
Q

allergic asthma cytokines

A

IL-4 IgE production
IL-5 eosinophil chemoattractant
IL-9 Th-2 response
IL-13 mucus production

63
Q

cell types and mediators allergic asthma

A

mast cell degranulation
- histamine
- leukotrienes
- prostaglandins

Th2 –> cytokines
- IL4 IgE
- IL5 eosinophils
- IL13 mucus

64
Q

nonallergic asthma cell types and mediators

A

Th17/IL17
Neutrophil infiltration

65
Q

charcot-leyden crystals

A

precipitated IgE
allergic asthma

66
Q

curshmann spiral

A

mucus plug
asthma, bronchiectasis

67
Q

ipatropium

A

anticholinergic/muscarinic antagonist
fast acting asthma tx

68
Q

montelukast

A

leukotriene inhibitor
asthma, aspirin-induced asthma

69
Q

salmeterol

A

LABA

70
Q

inhaled corticosteroids

A

fluticasone
budesonide

71
Q

omalizumab

A

anti-IgE

72
Q

mepolizumab

A

anti-IgE

73
Q

risk fx bronchiectasis

A

COPD
FBO
congenital obstruction
asthma
RA
Sjorgen
immunodeficiency
CF
PCD

74
Q

primary ciliary dyskinesia

A

PCD
dynein mutation
impaired cilia motility
bronchiectasis - infertility - possible situs inversus

75
Q

organism most often implicated in exacerbation of bronchiectasis

A

pseudomonas

76
Q

emphysema and smoking

A

smoking –> leukocyte release of proteases
emphysema = protease > antiprotease
centriacinar emphysema (most damage to area most directly exposed to smoke)

77
Q

A1AT histology

A

Periodic acid-shiff granules on liver biopsy

78
Q

A1AT path

A

alpha-1-antitrypsin deficiency
liver can’t release A1AT –> can’t reach lungs
lung antiprotease < protease –> emphysema
panacinar emphysema

79
Q

chronic bronchitis tx

A

SABA, LABA
SAMA, LAMA (beta-2)

e.g.,
albuterol, salmeterol
ipratropium, tiotropium

80
Q

organisms most implicated in COPD exacerbation

A

H flu
S pneum
Morazella catarrhalis

81
Q

empiric antimicrobials AECOPD

A

respiratory fluoroquinolone (levo or moxi)
or

amoxicillin or ceftriaxone
plus
macrolide e.g. azithromycin

82
Q

Honeycomb changes

A

Ip F

83
Q

IPF tx

A

Nintedanib
Pirfenidone

84
Q

Nintedanib

A

Tyrk-r blocker
Ipf
Slows progression

85
Q

Perfenidore

A

Antifibrotic
Inhibits tgf-b_induced collagen synthesis

86
Q

Hs pneumonitis-pfts

A

Restrictive pattern

87
Q

Acute Hs pneumonitis immunology

A

Type 3 Hs

88
Q

Subacute/chronic Hs pneumonitis immunology

A

Type 4
Th 1 and 17
→ progressive fibrosis

89
Q

Common antigens Hs pneumonitis

A

Moldy:
-Hay
- barley
- chees e
Dusty grain
Pigeon droppings
Tobacco plants
Chemicals- trimellitic anhydride, isocyanates
Cool mist humidifier

90
Q

Hs pneumonitis Tx

A

Antigen avoidance
Breathing mask
If severe- systemic steroids - short term
End stage- lung transplant

91
Q

Eggshell calcifications imaging

A

Silicosis

92
Q

Silicosis increased risk for _

A

Tb

93
Q

Cancers asbestosis

A

Most common: bronchogenic_,.carcinoma
Most specific - mesothelioma

94
Q

Pulmory-effusio causes

A
  • Ch f - increased hydrostatic pressure
    Pneumonia
    Liver disease
    Heart disease
    Kidney disease - low oncotic pressure
    Autoimmune disease
    Cancer

Infection and inflammation - vascular permeability

95
Q

TransUdate

A

Low proteinand cell content
From high hydrostatic pressure or low oncotic pressure

96
Q

Exudate

A

High protein and cell content
Vessel damage- inflammation, infection, malignant

97
Q

Thoracentesis

A

Pleural fluid analysis - transudate or exudate

98
Q

High triglycerides pleural fluid

A

> 110
Chylothorax
Thoracic duct injury
Chronic effusion

99
Q

Low glucose pleural fluid

A

<60
Inflammatory, malignant, infections

100
Q

Low ph pleural fluid

A

Nor mal 7.6
<7.3 infection, malignancies

101
Q

Tension PTX

A

PTX + shock
Dt very high air pressure → collapses SVC

102
Q

Good pasture Syndrome

A

RPG N with pulmonary manifestations
Ab vs bm

Alveolar hemorrhage
- hemoptysis
- anemia
-Pulmonary infiltrates
- high DLCO dt Hgb accumulation in alveoli

103
Q

Granulomatosis with polyangiitis

A

RPG N with pulmonary sx
Other symptoms also unlike good pasture - ent most common
Ab vs neutrophil - cANCA
Necrotizingvasculitis

Lung parenchyma l nodules
Interstitial lung disease
Possible alveolar hemorrhage

104
Q

Microscopic polyangiitis

A

Similar to granulomatous polyangiitis
But no gran. Formation and no nasal pharyngeal involvement.

105
Q

Eosinophilic granulomatous polyangiitis -

A

Similar to non-eosinophilic
But preceded by allergic sx
More gi involvement
Eventual heart involvement

106
Q

Pulmonary hypertension Tx

A

Endothelin receptor antagonists _ decrease pvr
-Bosentan
Prostacyclins - direct vasodilators -
- iloprost
- epoprosten ol
Pde-5 inhibitor - prolongs vasodilator effect of No
-Tadalafil

STEP1 (15 decks)

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