FA 1 Flashcards

1
Q

pulsus paradoxus - seen in

A
  1. cardiac teponade 2. asthma 3. obstructive sleep apnea

4. pericarditis 5. croup

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

asthma - histology

A
  1. smooth muscle hypertrophy
  2. Curschmann spirals: shed epithelium forms whorled mucus plugs
  3. Charcot - Leyden crystals: eosinophilic, hexagonal, double-pointed, needle-like crystal from breakdown of eosinophils in sputum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

asthma drugs

A
  1. β2 agonists (albuterol, salmeterol, formoterol)
  2. corticosteroids (fluticasone, budesonide)
  3. Muscarinic antagonists (ipratropium)
  4. Antileukotrienes (montelukast, zafirlukast, zileuton)
  5. omalizumab
  6. Methylxanthines (theophylline)
  7. Metacholine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

role of corticosteroids (fluticosine, budesonide) in asthma therpay
asthma - albuterol used in

A
  • 1st line therapy for chronic asthma

- during acute exacerbation

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

asthma - ipratropium vs tiotropium according to action

A

tiotropium is long acting

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

montelukast, zafirukast mechanism of action

A

block leukotriene receptor (CysLT1)

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

Zileuton mechanism of action / SE

A

5-lipoxygenase pathway inhibitor. Block conversion of arachnoid acid to leukotrienes
- hepatotoxic

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

adenosine receptor antagonists

A
  1. theophylline

2. caffeine

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

theophylline adverse effects

A
  1. cardiotoxicity
  2. neurotoxicity
    narrow therapeutic index
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

think asthma as a diagnosis when

A
  1. Recurrent episodes of wheezing
  2. Cough at night
  3. Coughing or wheezing after exercise
  4. Cough, wheezing, chest tightness after exposure to allergens or pollutants
  5. Colds “go down to the chest” or take longer than 10 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

inspiratory reserve volume (IRV)

A

air that can still be breathed in after normal inspiration (3.3L)

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

Expiratory reserve volume (ERV)

A

air that can be breathed out after normal expiration (1L)

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

Inspiratory capacity (IC)

A

inspiratory reserve volume (IRV) + tidal volume (TV)

3.8L

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

Vital capacity (VC)

A

Maximum volume of gas that can be expired after a maximal inspiration (4.8L)
inspiratory reserve volume (IRV) + tidal volume (TV) + Expiratory reserve volume (ERV)

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

Functional residual capacity (FRC)

A
Volume of gas in lungs after normal expiration (2.2L)
Residual volume (RV) + Expiratory reserve volume (ERV)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

minute ventilation (Ve)

A

total volume of gas that entering lungs per minute

Ve = tidal volume x respiratory rate

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

Alveolar ventilation (Va)

A

volume of gas per unit time that REACHES ALVEOLI

Va = (tidal volume - physiological dead space) x respiratory rate

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

situations that alter FEV1/FVC

A

decreased: obstructive lung disease
increased: restrictive lung disease

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

IRV is used during

A

exercise

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

Lung volumes that cannot be measured by spirometry

A
  1. residual volume
  2. Total lung capacity
  3. Functional residual capacity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Causes of increased Vital capacity

A

acromegaly

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

physiologic dead space equation

A

tidal volume (Vt) x (arterial PCO2- expired PCO2)/ arterial PCO2

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

physiologic dead space definition

A

anatomic dead space of conducting airways plus alveolar dead space
Volume of inspired air that does not take part in gas exchange

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

alveolar dead space distribution

A

apex of healthy lung is largest contributor of dead space

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

Physiologic dead space (per breath) normal

A

150 ml/breath

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

pathologic dead space

A

when part of the respiratory zone becomes unable to perform gas exchange (ventilated but not perfused)

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

Lung cancer - complication

A

mnemonic: SPHERE + dysphagia + phrenic nerve paresis - heart or pericardial invasion +pleural invasion
1. Superior vena cava syndrome 2. Pancoast tumor
3. Horner syndrome 4. Endocrine (paraneoplastic)
5. Recurrent laryngeal nerve compression (hoarseness)
6. Effusions (pleural or pericardial)

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

Lung cancer - risk factors

A
  1. smoking 2. secondhand smoking 3. radon 4. asbestos 5. family history 6. Asbestosis 7. Silicosis
  2. Coal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

primary lung cancer - types (small or non small?) / location

A
  1. small cell (oat cell) carcinoma - central
  2. adenocarcinoma (non-small) - peripheral
  3. Squamous cell carcinoma (non-small) - central
  4. Large cell carcinoma (non-small) - peripheral
  5. Bronchial carcinoid tumor (non-small) - central or peripheral
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

lung small cell (oat cell) carcinoma may cause/produce

A
  1. Cushing syndrome (ACTH) 2. SIADH
  2. antibodies against presynapitc Ca2+ channels (Lambert-Eaton myasthenic syndrome)
  3. or neurons (paraneoplastic myelitis/encephalitis, sabacute cerebellar degeneration)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

lung small cell (oat cell) carcinoma - gene amplification

A

MYC

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

lung small cell (oat cell) carcinoma - histology

A
  1. neoplasm of neuroendocrine Kulchitsky cells (small dark blue cells)
  2. chromogranin A positive
  3. undifferentiated (very aggressive)
  4. Neuron specific enolase positive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

lung squamous cell carcinoma - may cause/produce

A
  1. cavitation

2. hypercalcemia (produce PTHrP)

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

lung squamous cell carcinoma - CXR

A

Hillar mass arising from bronchus b

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

bronchial carcinoid tumor - histology

A

nests of neuroendocrine cells

chromogranin A positive

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

chromogranin A positive lung tumors

A
  1. bronchial carcinoid tumor

2. lung small cell (oat cell) carcinoma

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

bronchial carcinoid tumor - presentation/symptoms

A
  1. symptoms due to mass effect

2. carcinoid syndrome (flashing, diarrhea, wheezing)

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

lung Large cell carcinoma - treatment / it can secrete …

A
  1. less responsive to chemotherapy
  2. remove surgically
    - β-hCG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

MC primary lung cancer

MC lung cancer in non smokers

A

adenocarcinoma

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

lung adenocarcinoma activating mutations / paraneoplastic

A
  1. KRAS 2. EGFR 3. ALK

- hypertrophic osteorarthropathy (clubbing)

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

adenocarcinoma in siitu

A

bronchioarveolar subtype (hazy infiltrates similar pneumonia)

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

bronchioarveolar subtype - smoking

Bronchial carcinoid tumor - smoking

A

both no relationship

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

mesothelioma - risk factors

A

asbestosis

smoking is not a risk factor

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

mesothelioma - histology / RF

A
  • psammoma bodies
  • calretinin and cytokeratin (+) in almost all mesotheliomas, ((-) in most carcinomas)
  • RF: ASBESTOSIS (not smoking)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

pancoast tumor (superior sulcus tumor) may cause

A

Compression of locoregional structures:

  1. Horner syndrome
  2. Superior vena cava syndrome
  3. hoarseness
  4. sensorimotor deficits
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

superior vena cava syndrome - medical emergency because

A

it can raise intracranial pressure (if obstruction is severe)
–> headaches, dizziness, increased risk of aneurysm/rupture of intracranial arteries

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

Lung Ca - MC symptom

Lung Ca - single most common area of metastasis

A
  • cough (75%)

- brain

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

primary spontaneous pneumothorax is due to

A

rupture of apical blebs or cysts in tall, thin, young males

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

secondary spontaneous pneumothorax is due to

A
  1. diseased lung (bullae in emphysema, infections)

2. mechanical ventilation with use of high pressures (barotrauma)

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

thrombi pulmonary emboli - histology

A

lines of Zahn: interdigitating areas of pink (platelets, fibrin) and red (RBCs) found only in thrombi formed before death

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

lobar pneumonia - typical organisms

A
  1. S pneumonia
  2. Legionella
  3. Klebsiella
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Bronchopneumonia - typical organisms

A
  1. S. pneumonia
  2. S. aureus
  3. H. influenza
  4. Klebsiella
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

interstitial (atypical) pneumonia - typical organisms

A
  1. Viruses (influenza, CMV, RSV, adenovirus)
  2. Mycoplasma
  3. Legionella
  4. Chlamydia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

organism that causes BOTH Lobar and Bronchopneumonia

A

Klebsiella

S. pneumonia

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

bronchopneumonia - distribution

A

patchy distribution involving >= 1 lobe

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

walking pneumonia

A

interstitial (atypical) pneumonia –> generally follows a more indolent course

57
Q

interstitial atypical pneumonia - typical presentation

A

relatively mild URI symptoms

58
Q

lung abscess - organisms

A
  1. anaerobes (bacteroids, peptostreptococcus, fusobacterium)
  2. S aureus
  3. Klebsiella
59
Q

S. aureus - pneumonia type?

A

Bronchopneumonia (or lung abscess)

60
Q

H. infl - pneumonia type?

A

bronchopneumonia

61
Q

Lung abscess 2ry to aspiration is most often found in …. (location)

A

right lung:
upright –> basal segment of right lowr lobe
supine –> posterior segment of right upper lobe or superior segment of right lower lobe

62
Q

structure perforating diaphragm (an where)

A

T8: IVC
T10: esophagus vagus
T12: aorta, thoracic duct, azygos vein

63
Q

Screening test for fetal lung maturity

A
  1. lecithin/sphingomyelin ration in amniotic fluid –>
    - if more than 2 –> healthy
    - if less than 1.5 –> predictive of NRDAS
  2. foam stability test
  3. surfactant/albumin ratio
64
Q

Pulmonary surfactant synthesis by time

A

begins around week 26 of gestation, but mature levels are not achieved until around week 35

65
Q

hemoglobin (hb) - properties

A
  1. positive cooperativity

2. negative allostery

66
Q

hemoglobin (hb) - positive cooperativity

A

tetrameric Hb molecule can bind 4 02 molecules and has higher affinity for each subsequent O2 molecule bound

67
Q

methemoglobin vs normal hemoglobin - iron status

A

normal: resuced state Fe2+ (FERROUS)
methemoglobin: oxidized state Fe3+ (FERRIC)

68
Q

methemoglobin properties

A
  • it does not bind 02 as readily

- it has increased affinity for cyanide

69
Q

methoglobinemia may present with

A
  1. cyanosis 2. chocolate-colored blood
70
Q

methoglobinemia can can be treated with

A
  1. methylene blue

2. vitamin C

71
Q

how to treat cyanide poisoning (and the mechanism)

A

nitrites followed by thiosulfate

nitrites: hemoglobin –> methoglobin which bind cyanide
thiosulfate: to bind cyanide, forming thiocyanate , which is renally excreted

72
Q

substance that cause poisoning by oxidizing F2+ to F3+ (found in)

A
  1. nitrites (from dieaary intake or polluted/high altitude water)
  2. benzocaine
73
Q

methylene blue is used to

A

treat methoglobinemia

74
Q

1st generation H1 blockers - drugs

A
  1. diphenhydramine
  2. dimenhydrinate
  3. chlorpheniramine
75
Q

2nd generation H1 blockers - drugs

A
  • ADINE + cetirizine
    1. loratadine
    2. fexofenadine
    3. desloratadine
    4. cetirizine
76
Q

1st generation H1 blockers vs 2nd - used for

A

1st: 1. allergy 2. motion 3. sleep aid
2nd: allergy

77
Q

1st generation H1 blockers - toxicity

A
  1. sedation
  2. antimuscarinic
  3. anti-a-adrenergic
78
Q

2nd generation H1 blockers - toxicity

A

sedation (much less than 1st generation)

79
Q

pulmonary hypertension drugs - categories and drugs

A
  1. endothelin receptor antagonists –> BOSENTAN
  2. PDE-5 inhibitors –> SILDENAFIL
  3. Prostacyclin analogs –> EPOPROSTENOL, ILOPROST
80
Q

bosentan toxicity

A

hepatotoxicity

81
Q

pulmonary hypertensrion - prostacyclin analogs side effects

A
  1. flushing

2. jaw pain

82
Q

chronic bronchitis - pathology

A

hyperplasia of mucus-secreting glands –> Reid index >50%

83
Q

chronic bronchitis - definition

A

productive cough for >3 months PER YEAR (not necessarily consecutive) for >2 years

84
Q

bronchiectasia symptoms

A
  1. purulent sputum
  2. recurrent infections
  3. hemoptysis
  4. digital clubbing
85
Q

causes of poor ciliary motility

A
  1. smoking

2. kartegener syndrome

86
Q

bronchiectasia is associated with (like predisposition)

A
  1. bronchial obstruction
  2. poor ciliary motility (SMOKING, kartegener syndrome)
  3. cystic fibrosis
  4. allergic bronchopulmonary aspergillosis
87
Q

emphysema types - associations and area

A
  1. centriacinar: associated with smoking –> upper lobes

2. Panacinar: associated with α1 - antitrypsin –> lower lobes

88
Q

emphysema - diffusion capacity of CO test (and mechanism)

A

decreased diffusing capacity for CO resulting from destruction of alveolar walls

89
Q

blue bloaters vs pink puffer

A

blue: chronic bronchitis
pink: emphysema

90
Q

Restricted lung disease - poor breathing mechanics properties

A
  1. extrapulmonary
  2. peripheral hypoventilation
  3. normal A-a gradient
91
Q

Restricted lung disease - poor breathing mechanics –> situations (and causes)

A
  1. poor muscular effort (polio, myasthenia gravis)

2. poor structural apparatus (scoliosis, morbid obesity)

92
Q

Restricted lung disease - drug toxicity

A
  1. bleomycin 2. busulfan

3. amiodarone 4. methotrexate

93
Q

restrictive vs obstructive according FEV1

A

obstructive: FEV1 is MORE dramatically reduced compared to FVC
restrictive: FEV1 is LESS dramatically reduced compared to FCV

94
Q

pneumoconioses - types

A
  1. asbestosis
  2. Berylliosis
  3. Coal workers’ pneumoconiosis
  4. silicosis
95
Q

pneumoconioses (except berylliosi) - increased risk for

A
  1. cor pulmonale
  2. Caplan syndrome
  3. cancer
96
Q

Caplan syndrome

A

rheumatoid arthritis and pneumoconiases (coal, asbestosis, silicosis) with intrapulmonary nodules

97
Q

Asbestosis is associated with (exposure)

A
  1. shipbuilding
  2. roofing
  3. plumbing
98
Q

pathognomonic lesions of asbestosis (gross)

A

Ivory white, calcified supreadiaphragmatic and pleural plaques

99
Q

areas of asbestos plaques

A
  1. supreadiaphragmatic

2. pleural plaques

100
Q

carcinomas associated with asbestosis

A
  1. bronchogenic carcinoma (More common

2. mesothelioma

101
Q

berylliosis associated with (exposure)

A

berryllium in

  1. aerospace
  2. manufacturing industries
102
Q

lung Asbestosis - histology

A

ferruginous (asbestos) bodies: golden-brown fusiform rods resembling dumbbells, found in alveolar septum (visulized using PAS stain), often obtain by branchoalveolar lavage)

103
Q

ferruginous bodies are found in

A

alveolar septum

104
Q

berylliosis affects (area) / histology / treatment

A
  • upper lobes
  • noncaseating granoulomas in lung, hilar lymph nodes and systemic organs
  • occasionally responsive to steroids
105
Q

Coal workers’ pneumoconiosis is also known s / area

A

black lung disease

- upper lobes

106
Q

Coal workers’ pneumoconiosis - pathophysiology

A

prolonged coal dust exposure –> macrophages laden with carbon –> inflammation and fibrosis

107
Q

Anthracosis is caused by

A

mild exposure to carbon (collection of macrophages laden with carbon)

108
Q

Anthracosis - symptoms/found in

A

asymptomatic condition found in many urban dwellers exposed to sooty air

109
Q

Anthracosis - occupation

A

found in many urban dwellers exposed to sooty air

110
Q

Silicosis is associated with ….(occupation)

A
  1. foundries (factory that produces metal castings)
  2. sandblasting
  3. Mines
111
Q

Silicosis - pathophysiology

A

Macrophages respond to silica and release fibrogenic factors, leading to fibrosis. it is thought that silica may disrupt phagolysosomes and impair macrophages

112
Q

silicosis - increased risk for

A
  1. TB

2. bronchogenic carcinoma

113
Q

silicosis affects (area)

A

upper lobes

114
Q

silicosis - CXR

A

Eggshell calcification of hilar lymph nodes

115
Q

pneumoconiases that affect upper lobes

A
  1. coal workers’ pneumoconiosis
  2. Silicosi
  3. Berylliosis
116
Q

pneumoconiases that affect lower lobes

A

asbestosis

117
Q

which are the classicfication group of pulmonary hypertension

A
  1. pulmonary arterial hypertension (PAH)
  2. PH due to left heart disease
  3. PH due to lung disease or hypoxia
  4. chronic thromboembolic PH
  5. multifactorial PH
118
Q

multifactorial pulmonary hypertensions - causes

A
  1. hematologic disorders
  2. systemic disorders
  3. metabolic disorders
119
Q

pulmonary arterial hypertension (PAH) - causes

A
  1. idiopathic
  2. drugs
  3. connective tissue disease
  4. HIV infection
  5. portal hypertension
  6. congenital heart disease
  7. schistosomiasis
120
Q

pulmonary arterial hypertension (PAH) - idiopathic - pathophysiology

A

often due to inactivation mitation in BMPR2 gene –>

inhibits vascular SMCs proliferation

121
Q

neonatal respiratory distress syndrome - persistently low O2 tension - risk of

A
  1. PDA
  2. metabolic acidosis
  3. necrotizing enterocolitis
122
Q

neonatal respiratory distress syndrome - therapeutic supplemental of O2 can result in

A
  1. retinopathy of prematurity
  2. Intraventricular haemorrhage (brain)
  3. Bronchopulmonary dysplasia
123
Q

ARDS definition

A

clinical syndrome characterized by

  1. acute onset respiratory failure,
  2. bilateral lung opacities
  3. decreased Pa02/Fi02 ratio
  4. no HF
124
Q

ARDS management

A
  1. mechanical ventilation with LOW TIDAL VOLUMES

2. address underling cause

125
Q

sleep apnea - definition (and result)

A

repeated cessation of breathing > 10 seconds during sleep –> disrupted sleep –> daytime somnolence

126
Q

sleep apnea - PaO2 levels

A

normal during the day

noctural hypoxia

127
Q

sleep apnea - complications (how)

A

noctural hypoxia –>

  1. systemic/pulmonary hypertension
  2. arrhythmias (atrial fibrillation/flutter)
  3. sudden death
128
Q

sleep apnea - arrhythmia

A
  1. atrial fibrillation

2. atrial flutter

129
Q

sleep apnea - types

A
  1. obstructive sleep apnea
  2. central sleep apnea
  3. Obesity hypoventilation syndrome
130
Q

obstructive sleep apnea - associated with

A
  1. obesity

2. loud snoring

131
Q

obstructive sleep apnea - caused by

A
  1. excess parapharyngeal tissue in adults

2. adenotonsillar hypertrophy in children

132
Q

obstructive sleep apnea in children vs adults - is caused by

A

children: adenotonsillar hypertrophy excess parapharyngeal
adults: excess parapharyngeal tissue

133
Q

obstructive sleep apnea - treatment

A
  1. weight loss
  2. CPAP (continuous positive airway pressure)
  3. surgery
134
Q

central sleep apnea - due to

A
  1. CNS injury
  2. CNS toxicity
  3. opioids
  4. Heart failure
135
Q

Obesity hyperventilation syndrome - respiratory rate / BMI

A

decreased

>=30Kg/m2

136
Q

Obesity hyperventilation syndrome is also known as

A

Pickwickian syndrome

137
Q

Obesity hypoventilation syndrome - pathophysiology

A

BMI >=30Kg/m2 –> hypoventilation (decreased RR) –> decreased PaO2 and increased PaCO2 during sleep –> increased PaCO2 DURING WAKING HOURS (retention)

138
Q

Obesity hypoventilation syndrome - symptoms

A
  1. Poor sleep quality
  2. Sleep apnea
  3. Daytime sleepiness
  4. Depression
  5. Headaches
139
Q

Obesity hypoventilation syndrome - blood gases abnormalities

A
  1. increased PaCO2 during sleep
  2. decreased PaO2 during sleep
  3. Increased PaCO2 during waking hours (retention)