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5th year blocks > pulmonology > Flashcards

pulmonology Flashcards

1
Q

Lung volumes? (4)

A

Tidal volume: normal in/ex 500mL
Inspiratory reserve volume max in beside TV 3000mL
Expiratory reserve volume: max ex beside TV 1200mL
Residual volume: gas left in lungs after ex 1200mL

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2
Q

Lung capasities

A

Inspiratory capacity: tidal + IRV 3500ml
Functional residual capacity: ERV+RV 2400ml
Vital capacity: all air max in/ex 4700ml
Total lung capacity: 5700ml

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3
Q

what two parameters are measured in a spirometry?

A

tidal volume and air flow

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4
Q

what is FEV1 and FEC

A

FEV1: forced expiration air the first second
FEC is the total expired air during the test

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5
Q

what % during spirometry decides the lund capacity?

A

FEV1/FVC = should be > 70%

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6
Q

FEV1/FCV < 70% indicates

A

obstructive lung disease

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7
Q

Decreased PEFR indicates ( peak expiratory flow rate)

A

Bronchi/tracheal obstruction

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8
Q

decreased FEF 25% indicates

A

middle airway obstruction

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9
Q

decreased FEF 50% and 75% indicates

A

peripheral airway narrowing (smaller bronchi)

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10
Q

what is the limitations of the spirometry test?

A

only measures volume that can move so not RV - use body plethysmography for this

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11
Q

CO pulmonary test CI?

A

recent surgery
AMI
retinal displacement
pneumothorax

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12
Q

bronchodilator reversibility test

A

to diagnose asthma or differentiate between COPD and asthma

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13
Q

steps of bronchodilator revertability testing

A
  1. spirometry
  2. 400mcg salbutamol
  3. wait 15 min
  4. new spirometry
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14
Q

results of a bronchodilator reverasbility test?

A

if FEV1 > 200 ml post bronchodilator then it is asthma

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15
Q

when do we use a Bronchial provocation test?

A

if suspected asthma with a normal spirometry test

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16
Q

what do we give in a bronchial provocation test?

A

Methacholin mostly (or histamin, adenosin, bradykinin)

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17
Q

results of a bronchial provocation test?

A

if FEV1 decreases with > 20% most likely asthma

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18
Q

contraindications of bronchial provocation test?

A

Severe airway obstruction
FEV1 < 1L
Recent MI
Severe HT
Aortic aneurysm

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19
Q

what is measured during an ergo spirometry?

A

VO2 max (oxygen utilization)
CO2 production rate
minute ventilation
lung volumes

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20
Q

absolute CI of ergo spirometry?

A

coronary insufficiency
uncontrolled arrhythmia
Decompensated HF
Acute pulmonary edema
Valvular stenosis
Spo2 < 85%
ARF
Untreated thyrotoxicosis

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21
Q

In vitro allergy tests?

A

Tryptase in serum
Allergen-specific IgE
Toral IgE

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22
Q

In vivo allergy testing

A

skin prick test
skin scratch test
intradermal test

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23
Q

when is a in vivo allergy test positiv?

A

skin prick test: when wheal is > 3mm

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24
Q

types of sleep apnea

A

cental and obstructive

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25
Q

standardized screening questions

A

STOP BANG

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26
Q

diagnosis criteria of sleep apnea

A

Daytime fatigue + more then two of:
- Loud snoring
- Witnessed choking, gasping, apnea during sleep
- Diagnosis of HT

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27
Q

indications of ABG?

A

Gas exchange abnormalities
Acute resp failure
Cardiovascular diseases
Exercise test
Sleep disorders
Acid/base abnormalities
Emergency settings

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28
Q

Allen test before ABG

A

The Allen test is used to assess collateral blood flow to the hands, generally in preparation for a procedure that has the potential to disrupt blood flow in either the radial or the ulnar artery.

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29
Q

TB skin test

A

tuberculin injected under skin - 48-72h reaction means previously infected

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30
Q

TB speciment test?

A

Bronchoalveolar lavage
sputum
Aspirates from nasopharynx, endotracheal

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31
Q

latent TB treatment

A

Izoniazide for 9 months

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32
Q

TB treatment

A

RIPE
Rifampicin
Izoniazine
Pyrazinamide
Ethambutol

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33
Q

TB stain?

A

Zeil Neelsen staining (red microbes)

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34
Q

TB culture

A

Blood agar, chocolat agar and charcoal yeast, Lowenstein-Jensen
1-2 days to culture
1-2 days for susceptibility test

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35
Q

Pleural effusion Transudate vs Exudate

A

Transudate is hyper filtrated < 0.5 protein
Exudate is concentrated > 0.5 protein

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36
Q

physical examination of pleural effusion signs

A

Reduced chest expansion
Dull percussion
Quiet breathing sounds
Friction rub may be heard in inflammation

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37
Q

CXR in pleural effusion

A

PA view can detect only if over 200ml
LL view can detect > 50ml

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38
Q

DDx of pleural effusion

A

TB
Pneumonia
PE
malignancy
Rheumatoid arthritis
Hemothorax

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39
Q

what type of pulmonary effusion is most common in congestive HF, liver cirrhosis and hypoalbuminemia

A

Transudate

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40
Q

hemoptysis DDx

A

bronchial tumor
pneumonia
PE
Bronchiectasis
TB
Vasculitis
forging body

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41
Q

DDx of acute dyspnea

A

PTX
PE
AMI
Airway disease (COPD and Asthma exacerbation)
Metabolic acidosis
Hyperventilation syndrom

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42
Q

DDx of chronic dyspnea

A

Asthma
COPD
Parenchymal diseases (IPF, sarcoidosis, lymphagenitis, carcinomatosis)
Chest wall deformity
Myasthenia gravis
Anemia
Hypoxia

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43
Q

DDX of chest pain in pulmo disease

A

AMI
Pulmonary infarction
PE
pneumonia
PTX
Pericarditis
Autoimmune diseases
Fractured ribs

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44
Q

define chronic bronchitis

A

productive cough for at least 3 months each year for 2 years

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45
Q

define emphysema

A

permanent dilation of airspaces distal to terminal bronchioles caused by destruction of alveolar walls and pulmonary capillaries req. for gas exchange

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46
Q

exogenous causes of COPD

A

smoking
pollution

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47
Q

endogenous causes of COPD

A

a1-trypsin deficiency
developmental abnormalities
recurrent infections (Pneumonia, TB)
Premature
Primary ciliary dyskinesia
Ab deficiency (IgA)

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48
Q

Reid index

A

Ratio of the thickness of submucosal mucus secreting glands to the thickness between the epithelium and cartilage in the bronchial tree (whole wall)
If > 0.5 then chronic bronchitis

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49
Q

physiological processes involved in chronic bronchitis

A
  1. Increased neutrophils, macrophages and CD8+ cells
  2. overproduction of growth factor causing fibrosis, narrowing and emphysema
  3. Goblet cell proliferation and mucus hypersecretion
  4. impaired ciliary function
  5. SMC hyperplasia of small airways and capillary’s causing HT
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50
Q

explain the specific process og the emphysema in COPD

A

inactivation of protease inhibitors (a1-trypsin) causes increased proteases and elastase activity, loss of elastic tissue and lung parenchyma and loss of elastic recoil hence large spaces

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51
Q

two clinical appearances of COPD

A

pink puffers: emphysema
Blue bloaters: Chronic bronchitis

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52
Q

GOLD classification of COPD

A

1: MILD - FEV1 > 80%
2: MODERATE - FEV1 50-80%
3: SEVERE - FEV1 30-50%
4: VERY SEVERE - FEV1 < 30%

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53
Q

classification of emphysema?

A

Centriacinar (in the resp bronchiole)
Panacinar: (whole alveoli space)
Giant Bullous emphysema
Senile emphysema (airspace dilatation without alveolar wall destruction)

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54
Q

spirometry finding in COPD

A

Scooped curved during expiration
RV and TLC are abnormally high due to increased lung compliance and decreased recoil (air trapping)

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55
Q

3 pharmacological treatments if COPD

A
  1. bronchodilators
  2. Inhaled CS
  3. PDE4 inhibitors
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56
Q

SABA?

A

Salbutamol, fenoterol

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57
Q

LABA

A

Salmeterol, formeterol

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58
Q

SAMA

A

ipratropium bromide

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59
Q

LAMA

A

tiotropium bromide

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60
Q

inhaled CS?

A

budesonide
fluticasone
beclomethasone

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61
Q

PDE4 inhibitor

A

roflumilast

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62
Q

what is MRC?
What is it used in?

A

Modified medical research council dyspnea scale
Used in deciding pharmacological treatment of COPD

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63
Q

medication in severe refractory COPD

A

theophylline (adenosin receptor blocker and nonspecific PDE inhibitor)

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64
Q

when to give long term oxygen therapy in COPD

A

PaO2 < 55 mmHg
Sao2 < 88% at rest

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65
Q

target O2 saturation in COPD

A

90-93%

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66
Q

most common cause of AECOPD

A

rhinovirus
parainfluenza virus
RSV
Influenza
adenovirus

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67
Q

name bacteria causing AECOPD

A

hemophilus influenza
Maroxella
Strep. pneumonia

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68
Q

what drug can cause AECOPD

A

B-blockers

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69
Q

diagnosis of AECOPD

A

clinical presentation
imaging and other tests can be taken to find the cause

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70
Q

treatment of AECOPD

A

NIPPV with BiPAP
invasive mechanical ventilation in case of resp failure or shock
antibiotics
CS
Bronchodilators

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71
Q

define asthma

A

Chronic resp disease with bronchial hypersensitivity and episodic attacks

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72
Q

asthma pathophysiology

A

overproduction of Th2 cells causes overproduction of cytokines and activation of eosinophils inducing cellular response

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73
Q

How can aspirin induce asthma?

A

COX-1 inhibition - decreased PGE2 - Increased leukotrienes and inflammation and result in submucosal edema

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74
Q

lung sound on asculation in asthma?

A

hyperresonance
end expiratory wheezels
long expiration

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75
Q

spirometry asthma signs?

A

Decreased FEV1
decreased FEV1/FVC ratio

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76
Q

Mast cell stabilizers

A

cromolyn

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77
Q

Anti-IgE antibodies drug

A

omalizumab

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78
Q

treatment of Asthma

A

it depends on symptom frequency and the treatment is based on ICS+formeterol, then you up the dose depending on severity

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79
Q

step 5 treatment of asthma (Severe)

A

in severe cases you add a LAMA + Anti-IgE + high dose ICS and refer to phenotyping

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80
Q

what is acute ex. of asthma?

A

worsening of symptoms with change in baselin lung function

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81
Q

define status asthmatics

A

severe exacerbations of astma refractory to acute treatment

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82
Q

what are signs if resp failure in asthma exacerbation?

A

high PCO2 with normal pH and resp muscle fatigue

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83
Q

treatment of acute exacerbations asthma

A

ASTHMA
Albuterol (SABA)
Steroids
Humidified O2
Magnesium
Anticholinergics (SAMA)

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84
Q

Benefits of inhalers VS oral drugs?

A

inhalers:
- Rapid onset
- Smaller dose
- Better tolerance
- BUT more expensive

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85
Q

types of inhalers

A

Meter dose inhaler (MDI)
Spacer
Dry powder inhaler
Nebulizer

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86
Q

causes of community acquired pneumonia

A

Strep. pneumonia
Mycoplasma pneumonia
chlamydia pneumonia
Hemophilus influenza
klebsiella pneumonia
Acinetobacter
S. viridians from aspiration

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87
Q

how is the cough during pneumonia?

A

Productive purulent (yellow)

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88
Q

Auscultation findings during pneumonia?

A

Fine crepitation’s and crackles during first 2 weeks
Bronchial breath sounds
Decreased breathing sounds

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89
Q

How to decide treatment of pneumonia?

A

PORT classification

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90
Q

what are the PORT classes and their treatment?

A

PORT I: at home AB per os (amoxicillin-clavulonic acid)
PORT II-III: at home AB per os some req. late hospitalization
PORT III-IV: iv AB combo + hospital (amoxicillin-clav + Macrolide)
PORT IV-V: iv AB combo + resp IC (amoxicillin-clav + Macrolide)

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91
Q

what is nosocomial pneumonia?

A

hospital aq. with onset > 48h after admission

92
Q

causes of nosocomial pneumonia

A

Enterobacter
pseudomonas
Acinetobacter
Hemophilus
Fusobactam
Bacteroids

93
Q

nosocomial pneumonia treatment

A

rec. prolonged IV treatment with typically used amoxiclav, ceftriaxone, piperacillin-tazobactam, carbapenem

also consider MRSA coverage

94
Q

define lung abscess

A

localized collection of puss and necrosis within lung parenchyma caused by microbial infection
- Primary: in normal lung parenchyma
- Secondary: immunocompromised patients

95
Q

etiology of lung abscess

A

Bacterial: Fusobacterium, Prevotella, Bacteroids, Viridans, aureus
Fungal: Aspergillus, cryptococcus, histoplasma
Parasite: Entamoeba, paragonimus

96
Q

symptoms of lung abscess

A

fever
cough with production of foul smell
pleuritic pain
fatigue
hemoptysis
anorexia
night sweats

97
Q

immediate treatment of lung abscess?

A

dont wait for culture
start empiric AB asap with anaerobic coverage (ampicillin/carbapenems)

98
Q

what is empyema

A

accumulation of puss in pleural cavity

99
Q

etiology of empyema

A

pneumonia
infected hemothorax
ruptured abscess
esophageal tear
thoracic trauma

100
Q

classification of empyema

A

Stage 1: exudative
Stage 2: fibropurulent
Stage 3: Organized

101
Q

what AB is not used in empyema

A

aminoglycosides due to pore pleural bioavailability

102
Q

empyema treatment AB?

A

2nd/3rd gen. cephalosporins + metronidazole or clindamycin

103
Q

first line ab in TB

A

RIPE
Rifampin 6m
Isoniazid 6m
pyrazinamide 2m
Ethambutol 2m

104
Q

ab in drug resistante TB

A

aminoglycosides
fluoroquinolones
cycloserine
para-aminosalicylic acid

105
Q

two lung cancer types

A

Small cell lung cancer (only 1 type) 20%
Non-small cell lung cancer (many subtypes) 80%

106
Q

cell type in SCLC

A

Neuroendocrine
Anaplastic

107
Q

cell type in NSCLC

A

Squamous epithelium 45%
Adenocarcinoma 20%
Large cell carcinoma 15%

108
Q

cell type of origin in SCLC

A

Kulschitzky cells

109
Q

treatment of SCLC

A

Chemo + radio

110
Q

treatment of NSCLC

A

dependent on the stage of the disease
I-IIIa surgery
IIIb-IV chemo + radio

111
Q

steps in diagnosis lung cancer

A
  1. smoking
  2. symptomes
  3. chest x-ray
  4. CT
  5. histology (sputum cytology + bronchoscopy)
112
Q

how often is NSCLC operable?

A

10-20% of cases

113
Q

what is the cure rate in NSCLC

A

30% cured
70% relapse

114
Q

what is the cure rate in SCLC

A

10% cured
90% relaps

115
Q

can SCLC be surgically removed?

A

no, only radio+chemo

116
Q

pleural tumor?

A

mesothelioma, very rare, might also be seen in pericardium and peritoneum. 1 year survival

117
Q

cause of mesothelioma?

A

in majority of cases there has been exposure to asbestos

118
Q

Dx of pleural cancer?

A

pleurocentesis
CXR and CT
Laparoscopy - biopsy

119
Q

treatment of mesothelioma?

A

radio + chemo
surgery (pleurectomy) of it causes severe lung dysfunction

120
Q

symptoms of SCLC

A

constitutional symptoms (weight loss, fever, weakness)
SVC syndrom
Hoarseness (r. laryngeal n. palsy)
dyspnea (phrenic n. palsy)
Dullness percussion
dysphagia (esophageal compression)

121
Q

treatment of SCLC

A
  1. surgery NOT recommended
  2. stage I-III cisplatin/carboplatin 6 cycles + radio after 3rd cycle
  3. stage IV 4-6 cycles + 4 cycles of topotecan + cyclophosphamide-vincristin
122
Q

paraneoplastic syndrom in SCLC

A

1.cachexia
2. thrombocytosis DIC
3. hypercoagulation
4. dermatomyositis
5. acanthosis nigricans
6. Cushing’s
7. SIAD
8. Peripheral neuropathy
Lambert-Eton syndrom

123
Q

classification of pneumothorax

A
  1. Spontaneous (primary/secondary/recurrent)
  2. Traumatic PTX
  3. Tenson PTX
124
Q

Define tension PTX

A

one way air entry (like a valve) air enters upon inspiration but can’t exit during expiration causing pressure build up

125
Q

treatment of tension PTX

A

Resp support and treat dyspnea FIRST
then decompression

126
Q

Cell type origin in NSCLC SCC

A

metaplasia of squamous cells

127
Q

Cell type of origin in NSCLC ADC

A

Pneumocyte II cells

128
Q

define idiopathic pulmonary fibrosis

A

irreversible fibrosis and impaired pulmonary function. the most common ILD

129
Q

clinical presentation of IPF

A

progressive dyspnea (first at exertion then also at rest)
non-productive cough
crackles (later on wheezing)
dyspnea
fatigue
cyanosis
clubbing

130
Q

histopathology in IPF

A

Honeycomb appearance
Ground glass opacification with superimposed reticular abnormalities
Bibasal subpleural distribution
REMEMBER: other causes must be excluded for this to be IPF

131
Q

IPF treatment

A

stop smoking
transplant
supportive O2 therapy
antifibrotic agents (pirfenidone + nintedanib)

132
Q

define sarcoidosis

A

systemic condition characterized by non-caseating granulomatous inflammation in lungs and lymph

133
Q

Pathophysiology of sarcoidosis

A

a) T and B cell dysfunction
b) immune hyperactivity and inflammation
c) granuloma formation
d) fibrosis and damage of organ tissue
e) calcium dysregulation (due to hyper ph.)

134
Q

what is a granuloma composed of?

A

Epithelioid cells and macrophages in the center
Lymphocytes and fibroblasts around

135
Q

acute sarcoidosis symptoms

A
  1. sudden
  2. fever, malaise, weight loss
  3. dyspnea, cough, chest pain
  4. arthritis, anterior uveitis, erythema nodosum
136
Q

Cronic sarcoidosis symptoms

A
  1. lupus pernio
  2. lymphadenopathy
  3. bilateral hilar lymphadenopathy
  4. dyspnea + cough
  5. hepatomegaly/splenomegaly
  6. scar sarcoidosis
  7. symmetrical arthritis
  8. myalgia
  9. cystic bone lesion of distal phalanges
137
Q

sarcoidosis treatment

A

1st line: glucocorticoids
2nd line: immunosuppressants (methotrexate)
Anti-malarian drugs
Lung transplant

138
Q

prognosis of sarcoidosis?

A

70% have spontaneous remission
but increased calcium is ass. with poor prognosis

139
Q

define pulmonary HT

A

mean arterial pressure > 20 mmHg

140
Q

subtypes of pulmonary HT

A

precapillary HT
postcapillary HT
pulmonary arterial HT

141
Q

Etiology of PHT

A

Divided into groups
G1 Pulmonary arterial HT
G2 LHF
G3 Chronic lung disease
G4 Pulmonary arterial obstruction
G5 Unclear multifactorial

142
Q

diagnosing PHT

A

Trans thoracic echo and look for
- tricuspid regurgitation velocity
- RV pressure overload
- RV failure
- Underfilled left heart
-

143
Q

vasodilators in pulmonary HT

A

Calcium channel blockers: First-line pulmonary vasodilator

144
Q

define resp failure

A

acute or chronic inability of the respiratory system to maintane adequate gas exchange

145
Q

types of resp failure

A

Type 1: Hypoxic SpO2 < 60 mmHg
Type 2: Hypercapnic PaCO2 > 50 mmHg

146
Q

causes of resp failure

A
  1. impaired ventilation
  2. Airway obstruction
  3. impaired gass exchange
  4. VQ missmatch
147
Q

how to increase ventilation on oxygen support?

A

Increase RF or tidal volume

148
Q

how to increase oxygenation on resp support

A

increase FiO2 and increase PEEP

149
Q

Sleep apnea breathing events

A

apnea (complete stop for > 10 sec)
Hypoapnea (reduced airflow by > 30% for > 10 sec
Respiratory effort-related arousal (wake up due to increased resp effort)

150
Q

cause of obstructivee sleep apnea

A

collapse of pharyngeal muscle during sleep causing obstruction

151
Q

pathophysiology of sleep apnea (Obstructive)

A

apnea - decreased SpO2 - increased pCO2 - hypoxic pulmonary vasoconstriction - PHT - increase sympathetic activity and secondary HT

152
Q

treatment of obstructive sleep apnea

A
  1. PAP (CPAP/BiPAP)
  2. oral appliances (devices worn during sleep to keep mandible in place)
  3. Upper airway modifications (surgery if ex surgical dilation, uvuloplasty)
153
Q

pulmonary embolism etiology?

A

DVT
Fat embolism
Air embolism
amniotic fluid embolism
Bacterial embolism
tumor

154
Q

Vichows triad

A

endothelial damage
venous stasis
hypercoagulability

155
Q

most common site of DVT

A

iliac vein

156
Q

Wells score on PE

A

midl risk: < 2
moderate risk: 2-6
high risk: > 6

157
Q

imaging in PE

A

CT angiography
Echo
VQ scan

158
Q

hemodynamically stable vs unstable?

A

systolic blood pressure < 90 unstable
systolic blood pressure > 90 stable

159
Q

when is PE excluded?

A

Wells score < 4
Negative D dimer
Hemodynamically stable

160
Q

thrombolytic therapy?

A

tPA Alteplase (most used) and streptokinase/urokinase infusion for 24h

161
Q

Anticoagulants PE

A

Heparin IV 5000 units bolus + 1000-2000 units/hour infusion
Warfarin for 3w to 6 months

162
Q

recurrence of PE

A

without anticoagulants recurrence is 10% within first year

163
Q

normal O2 demand

A

4L/min/kg

164
Q

normal O2 values

A

PaO2 90-100mmHg
SatO2 > 95%

165
Q

O2 supplement method?

A

Nasal cannula
Simple face mask
Venturi mask
non-reservoir

166
Q

two classes og pulmonary edema?

A

cardiologic cause
non-cardiologic cause (pulmonary vs Non-pulmonary)

167
Q

imaging findings in the two types of pulmonary edema

A

Cardiogenic: Central edema, pleural effusion, enlarged heart
Non-cardiogenic: Patchy and peripheral edema, consolidations

168
Q

what is the gold standard to determine cause of pulmonary edema?

A

Pulmonary artery catheterization

169
Q

diuretics in pulmonary edema?

A

furosamide

170
Q

drug do reduce PCWP and cardiac filling pressure

A

Nesiritide

171
Q

define bronchiectasis

A

irreversible abnormal dilation in the bronchial tree caused by cycles of inflammation leding to mucous plugging and airway destruction

172
Q

etiology of bronchiectasis

A

disorders causing mucous plug or inflammation, bronchial narrowing

173
Q

Cystic fibrosis

A

AR disorder of defect cystic fibrosis transmembrane conductance regulator protein (CFTR) Cl channel doesn’t work

174
Q

what happens to mucous layers in organs when CF

A

normally Cl goes out of the cell and in the mucous it attrachs H2O keeping the mucous nice and thin. Not happening in CF and mucous gets hard and sticky

175
Q

cause of CF

A

mutation on ch 7 at the Delta F508 gene causing absence of phenylalanin and missfolding of the CFTR protein

176
Q

what happens in sweat glands in CF

A

here there is no REABSORPTION of Cl causing more NaCl to be excreted through the sweat

177
Q

GI complication of CF

A

pancreatitis
cholelithiasis
meconium ileus baby
exocrine pancreas dysfunction
CF related DM
intestinal obstruction
rectal prolaps

178
Q

Pulmonary complication of CF

A

COPD
Chronic sinusitis
recurrent chronic cough
airway obstruction
barrel chest
hemoptysis
chronic resp insufficiency

179
Q

urinary complication of CF

A

frequent stones
frequent UTI

180
Q

musculoskeletal complication of CF

A

frequent fractures
kyphoscoliosis

181
Q

pharmacological treatment of cystic fibrosis

A

High dose ibuprofen
CS
SABA LAMA
N-acetylcystein
Mucolytics

182
Q

define a1-trypsin deficiency

A

accumulation of a defect a1T protein due to mutation in SERPINA1 gene

183
Q

what is the normal function of a1-anti trypsin

A

protect cells against degradation by neutrophil elastase

184
Q

effect on liver in a1-anti trypsin deficiency

A

accumulation of the protein
hepatocyte destruction
cirrhosis
hepatitis

185
Q

effect on lungs in in a1-anti trypsin deficiency

A

uninhibited neutrophil elastase activity
destruction of parenchyma and pancellular emphysema

186
Q

diagnosis of a1-anti trypsin deficiency

A

Serum low levels
electrophoresis no peak
CXR
Chest CT
Liver biopsy: spherical inclusion bodies

187
Q

treatment in in a1-anti trypsin deficiency

A

treat symptoms
replacement if severe
liver transplant

188
Q

hypersensitivity pneumonitis

A

HS reaction following exposure to allergen ass. with interstitial lung disease

189
Q

type of HS in hypersensitivity pneumonitis

A

mix of type III and type IV

190
Q

most common source of allergen in hypersensitivity pneumonitis

A

actinomycete spores

191
Q

hypersensitivity pneumonitis stages

A

acute 4-8h
subacute weeks-months
chronic months and after

192
Q

hypersensitivity pneumonitis Dx

A

positive serology IgG and IgA or IgM
CXR
BAL (lymphocyte predominance
Lung Biopsy

193
Q

Eosinophilic pulmonary disease (loefflers)

A

accumulation of eosinophils in the lung due to certain infections or allergic reactions to drugs. Mild and passing symptoms

194
Q

diseases than can lead to need of lung transplant

A
  1. COPD
  2. Idiopathic pulmonary fibrosis
  3. genetic disorders such as CF a1 deficiency
  4. sarcoidosis
  5. IPAH
  6. lymphangio leio myomatosisi
195
Q

absolute contraindications of lung transplant

A

Malignancy the last 2y
Chronic advanced illness (heart, renal, liver)
Uncontrolled or untreatable pulmonary or ex. pulmonary infection
Poor cardiac function
Acute medical conditions (sepsis, MI, Liver failure)
Uncontrolled bleeding
HIV
Psychiatric problems
BMI > 35
Active alcohol, tobacco or substance use

196
Q

smoking cessation model

A

5A’s
Ask
Advise
Assess
Assist
Arrange

197
Q

Nicotin replacement

A

patches
chewing gum
sublingual tablets
nasal spray/inhalers

198
Q

Non-nicotine replacement

A

Bupropion: antidepressant reduce smoking desire
Varenicline: nAchR agonist releaving withdrawal

199
Q

what is a invasive ventilation

A

where we create a airway aith a tube

200
Q

typesk of masks

A

full face mask
total face mask
nasal mask
nasal pillows
mouth piece
helmet

201
Q

complication of NI ventilation

A

air leaks
aspiration pneumonia
ventilation ass- lung injury (barotrauma)
severe gastric distension
skin irritation
mucus plugging
mucosal dryness
nasal bridge ulcerations

202
Q

what is Fi O2
What is the value of air breathing in?

A

The amount of oxygen deliveres
In air 21%

203
Q

in ventilation what do to with a person with hypoxemic resp failure?

A

increase FiO2 or increase mean airway pressure to open collapsed alveoli

204
Q

in ventilation what do we to with a person with hypercapnic resp failure

A

increase tidal volume or minute ventilation

205
Q

types of NI ventilation

A

CPAP
BiPAP

206
Q

Define CPAP

A

continuous positive pressure flow during breath cycle
used in hypoxemic resp failure

207
Q

function of pleura

A

regulate pressure inside and outside the lungs and no friction with chest wall

208
Q

fluid in pleural space

A

8-10ml

209
Q

what is in the pleural fluid

A

electrolytes
albumin
macrophages
glucose
mesothelial cells
lymphocytes

210
Q

chest deformities

A

Barrel chest
Pectus Excavatum (funnel chest) (sternum inwards)
Pectus Carinatum (pigeon chest) (sternum outwards)
Kyphoscoliosis

211
Q

what does the pneumocytes do`

A

type I: lines alveoli
type II: produce surfactant

212
Q

how thick is alveoli

A

0.1-0.2mm in diameter

213
Q

vesicular breathing sound

A

soft, quiet
Long in/short out

214
Q

Bronchovesicular breathing sounds

A

intermediate loud
same in and out

215
Q

Bronchial breathing sounds

A

loud
short in/long out

216
Q

Tracheal breathing sounds

A

very loud
same in and out

217
Q

what location is a stridor coming from?

A

from the trachea and must not be mistaken for lung sound

218
Q

diseases with hypre resonance lung sound

A

asthma
COPD
Pneumothorax

219
Q

contraindication of chest X-ray

A

pregnancy

220
Q

X-ray views

A

anteroposterior (AP)
posteroanterior (PA)
lateral (LL)

221
Q

when to do a HRCT in lung diseases

A

very thin slides so used if parenchymal lung disease ex. interstitial lung disease involving the acini

222
Q

size of slice in a HRCT

A

1-2mm

223
Q

What is the main indication for ventilation perfusion scintigraphy?

A

A ventilation and perfusion scan is most often done to detect an acute pulmonary embolus (blood clot in the lungs). It is also used to: Detect abnormal circulation (shunts) in the blood vessels of the lungs (pulmonary vessels) Detect abnormal circulation from multiple old blood clots (chronic thromboembolic disease)

224
Q

what is used on PET CT

A

18-flyorodeoxyglucose

225
Q

false positives in PET CT

A

inflammation
metformin use
active brown adipose tissue
high physiological uptake in the brain

226
Q

causes of non-productive cough

A

ACEI
Emphysema
Cardiac disease
Pulmonary fibrosis

227
Q

chough acute vs chronic

A

less then 3w is acute
more then 8w is chronic

5th year blocks (14 decks)

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