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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
Allergic rhinitis Tx
1-intranasal steroids 2- antihistamines 3-cromolyn
26
Oral antihistamines 2nd gen
Cetirizine Loratadine Fexofenadine
27
Intranasal antihistamines
Azelastine Olopatadine
28
Cromolyn
Prevents mast cell degranulation Allergies Intranasal
29
Dominant cell type allergic rhinitis
Mast cells (not eosinophils)
30
Most common agent pharyngitis
Adenovirus
31
GAS pharyngitis Tx
Penicillin Reduces rheumatic fever incidence but not psgn
32
Gonorrhea Tx
Ceftriaxone
33
Chlamydia t x
Azythromycin - macrolide Doxy
34
Tonsillitis agents
Adenovirus Gas Mono
35
Epiglottit.is agents
H flu type B - vaccine - gram neg coccobacill: Strep Staph
36
Examining epiglottis
Don't in kids-can make it worse X-ray
37
Croup
Larynx and trachea inflammation Parainfluenza - most common Rsv Adenovirus Flu virus Kids <3 Barking cough "Steeple sign' X-ray
38
Severe croup Tx
Corticosteroids Inhaled epinephrine Heliox Sometimes intubate
39
Odynophagia
Painful swallowing Common in pharyngitis
40
Tonsillitis is u sually which tonsils
Palatine Sometimes pharyngeal aka adenoids
41
Visual cue bacterial vs viral pharyngitis
Tonsillar exudate Don't give abx if none but still send cultures
42
pulmonary capillary wedge pressure
approximates pressure in left atrium normal in ARDS increased in CHF
43
histology ARDS
hyaline membranes= diffuse endothelial damage
44
criteria ARDS
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
triggers ARDS
= 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
signs ARDS
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
ventilation ARDS
almost always needed settings: high PEEP - prevents alveolar collapse low LTVV (low tidal volume ventilation)
48
transient tachypnea of the newborn
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
newborn respiratory distress syndrome
any delivery stage generally lack of surfactant risk: - prematurity - multifetal pregnancies - maternal diabetes - genetic mutations surfactant
50
vasodilation after birth
O2 --> vasodilation in lungs alveolar collapse --> no vasodilation, further impedes gas exchange
51
grunting newborn
always dt respiratory distress partial glottal closing compensatory: increases airway pressure, stents airways, increases functional residual capacity impending respiratory failure
52
NRDS X-ray
ground glass opacities
53
NRDS tx
antenatal dexamethasone exogenous surfactant (direct to lung via brief intubation) CPAP O2 severe: inhaled NO (decreases pulmonary vascular resistance)
54
FEV1/FVC normal and path
normal = 80% obstructive < 70% restrictive = normal to high dt low TLC; FEV1 and FVC both decreased (FEV1 ≥ FVC)
55
PV loop normal and path
56
alpha-1-antitrypsin deficiency
emphysema dt failure to destroy destructive elastases young onset, usually few risk fx, usually family hx
57
bronchiectasis
bronchial necrosis and inflammation dilation and dysfunction abnormal mucous clearance e.g. CF
58
pneumoconiosis
fibrosis d/t foreign body scarring e.g. asbestos, coal dust, silica (sand)
59
drug induced ILD
amiodarone (antiarrythmetic) busulfan (alkylating chemo; CML, HSCT) bleomycin (antitumor antibiotic)
60
extrinsic causes RLD
ascites scoliosis/kyphosis other scmpression of thoracic space
61
digital clubbing
often associated with hypoxemia, restrictive lung disease
62
allergic asthma cytokines
IL-4 IgE production IL-5 eosinophil chemoattractant IL-9 Th-2 response IL-13 mucus production
63
cell types and mediators allergic asthma
mast cell degranulation - histamine - leukotrienes - prostaglandins Th2 --> cytokines - IL4 IgE - IL5 eosinophils - IL13 mucus
64
nonallergic asthma cell types and mediators
Th17/IL17 Neutrophil infiltration
65
charcot-leyden crystals
precipitated IgE allergic asthma
66
curshmann spiral
mucus plug asthma, bronchiectasis
67
ipatropium
anticholinergic/muscarinic antagonist fast acting asthma tx
68
montelukast
leukotriene inhibitor asthma, aspirin-induced asthma
69
salmeterol
LABA
70
inhaled corticosteroids
fluticasone budesonide
71
omalizumab
anti-IgE
72
mepolizumab
anti-IgE
73
risk fx bronchiectasis
COPD FBO congenital obstruction asthma RA Sjorgen immunodeficiency CF PCD
74
primary ciliary dyskinesia
PCD dynein mutation impaired cilia motility bronchiectasis - infertility - possible situs inversus
75
organism most often implicated in exacerbation of bronchiectasis
pseudomonas
76
emphysema and smoking
smoking --> leukocyte release of proteases emphysema = protease > antiprotease centriacinar emphysema (most damage to area most directly exposed to smoke)
77
A1AT histology
Periodic acid-shiff granules on liver biopsy
78
A1AT path
alpha-1-antitrypsin deficiency liver can't release A1AT --> can't reach lungs lung antiprotease < protease --> emphysema panacinar emphysema
79
chronic bronchitis tx
SABA, LABA SAMA, LAMA (beta-2) e.g., albuterol, salmeterol ipratropium, tiotropium
80
organisms most implicated in COPD exacerbation
H flu S pneum Morazella catarrhalis
81
empiric antimicrobials AECOPD
respiratory fluoroquinolone (levo or moxi) or amoxicillin or ceftriaxone plus macrolide e.g. azithromycin
82
Honeycomb changes
Ip F
83
IPF tx
Nintedanib Pirfenidone
84
Nintedanib
Tyrk-r blocker Ipf Slows progression
85
Perfenidore
Antifibrotic Inhibits tgf-b_induced collagen synthesis
86
Hs pneumonitis-pfts
Restrictive pattern
87
Acute Hs pneumonitis immunology
Type 3 Hs
88
Subacute/chronic Hs pneumonitis immunology
Type 4 Th 1 and 17 → progressive fibrosis
89
Common antigens Hs pneumonitis
Moldy: -Hay - barley - chees e Dusty grain Pigeon droppings Tobacco plants Chemicals- trimellitic anhydride, isocyanates Cool mist humidifier
90
Hs pneumonitis Tx
Antigen avoidance Breathing mask If severe- systemic steroids - short term End stage- lung transplant
91
Eggshell calcifications imaging
Silicosis
92
Silicosis increased risk for _
Tb
93
Cancers asbestosis
Most common: bronchogenic_,.carcinoma Most specific - mesothelioma
94
Pulmory-effusio causes
* Ch f - increased hydrostatic pressure Pneumonia Liver disease Heart disease Kidney disease - low oncotic pressure Autoimmune disease Cancer Infection and inflammation - vascular permeability
95
TransUdate
Low proteinand cell content From high hydrostatic pressure or low oncotic pressure
96
Exudate
High protein and cell content Vessel damage- inflammation, infection, malignant
97
Thoracentesis
Pleural fluid analysis - transudate or exudate
98
High triglycerides pleural fluid
>110 Chylothorax Thoracic duct injury Chronic effusion
99
Low glucose pleural fluid
<60 Inflammatory, malignant, infections
100
Low ph pleural fluid
Nor mal 7.6 <7.3 infection, malignancies
101
Tension PTX
PTX + shock Dt very high air pressure → collapses SVC
102
Good pasture Syndrome
RPG N with pulmonary manifestations Ab vs bm Alveolar hemorrhage - hemoptysis - anemia -Pulmonary infiltrates - high DLCO dt Hgb accumulation in alveoli
103
Granulomatosis with polyangiitis
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
Microscopic polyangiitis
Similar to granulomatous polyangiitis But no gran. Formation and no nasal pharyngeal involvement.
105
Eosinophilic granulomatous polyangiitis -
Similar to non-eosinophilic But preceded by allergic sx More gi involvement Eventual heart involvement
106
Pulmonary hypertension Tx
Endothelin receptor antagonists _ decrease pvr -Bosentan Prostacyclins - direct vasodilators - - iloprost - epoprosten ol Pde-5 inhibitor - prolongs vasodilator effect of No -Tadalafil

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