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Pulmonology > review > Flashcards

review Flashcards

1
Q

what happens to the airways in bronchiectasis?

A

they are permanently dilated and instead of seeing tapering of them we actually see them get bigger

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2
Q

mecocium ileus

A

clinical feature of CF

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3
Q

laboratory CF

A
  1. sweat chloride
  2. genetic testing for CTFR
  3. nasal trnasepithelial potential difference
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4
Q

CF tx.

A
  1. chest physical therapy
  2. antibiotics
  3. nebulized DNase
  4. Nebulized 7% saline
  5. bronchodilators but not an anti-cholinergic which causes slowing of the gut
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5
Q

no benefit for CF tx.

A
  1. inhaled steroids
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6
Q

prednisone in CF

A

benefit but risk outweighs as well as nsaids

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7
Q

hallmarks of asthma a

A
  1. airway inflammation
  2. airway hyperresponsiveness
  3. airflow obstruction
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8
Q

early asthma phase

A

mast cell driven in releasing histamine resulting in bronchospams

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9
Q

late asthma phase

A

cytokine and eosinophil driven leading to not onyl bronchospasm but also edema and inflammation

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10
Q

classic triad of asthma

A
  1. intermittent wheeze
  2. cough
  3. dyspnea
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11
Q

nocturnal asthma

A

lung function declines early morning driven to to decrease in catecholamines and increase in leukotriens and inflammatory cells

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12
Q

EIB

A

maybe there is water loss inducing an increases in tonicity

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13
Q

EIB treatment

A
  • Beta-2 agonist before exercise

- exercise a little before to get warmed up

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14
Q

ILD can bypass inflammatory pathway?

A

yep

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15
Q

ground glass opacities show ______ and can be treated with

A

acute and can be treated with steroids

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16
Q

honecombing show _______ and it is usually treated with

A

chronic but it is hard to treat… too late

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17
Q

reticular nodules are

A

infection

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18
Q

Exaggerate immune response to unidentified Ag (increase CD4)

A

sarcoidosis

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19
Q

Type 1 RADS

A

hypoxemic due usually to either a V/Q or shunt

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20
Q

acute RADS what do we see

A

increase catecholamines

- carotid body detects and increases respiratory rate and thus ventilation

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21
Q

chronic RADS

A

increases in erythropoetin leading to icnrease in gemoglobi n and thus increase in o2 concentration

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22
Q

Type II RADS

A

hypercapcnic

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23
Q

acute Type II rads

A

decrease in Ph leading to high CO2 narcosis

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24
Q

chronic type II rads

A

increase in renal bicarb. leading to increase in Ph

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25
Q

how much do you extract O2

A

about 25%

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26
Q

what happens if you can no longer compensate and extract the O2?

A

consumption drops and leads to acute organ failure

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27
Q

when do we thinking of dead space

A

hypercapnia

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28
Q

hypercapnia respiratory failure

A
  • increase in dead space
  • increase in VCO2
  • decrease in resp. drive
    decrease in resp. pump
  • increase in work of breathing
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29
Q

HFNC is used for

A

hypoxemia not a ton of ventilation but will help increase WOB

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30
Q

what happens with too much O2

A

acute lung injury leading to increased dead space, abnromal resp. drive and haldane effect

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31
Q

what can happen with supplemental O2 with atelectasis

A

washout of N2 from alv and venous blood accelerates resorption of air leading to resorption atelectasis

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32
Q

when should give non-invasive ventilation

A
  • acute resp failure with COPD

- acute cardiogenic pulm. edema, pneumonia

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33
Q

Refractory Hypoxemic Respiratory Failure

A

shunt

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34
Q

Ventilatory (Hypercapnic) Respiratory Failure

A

Elevated Work of Breathing
Respiratory Muscle Weakness/Endurance
Insufficient Respiratory Drive

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35
Q

all what must be present in ARDS

A
  1. Acute Onset: respiratory symptoms within one week of known clinical insult
  2. Abnormal CXR or CT: bilateral opacities c/w pulmonary edema, not fully explained by other processes
  3. Respiratory Failure: not fully explained by fluid overload or CHF
  4. Hypoxemia:
    PaO2/FiO2 <300
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36
Q

what happens in ARDS

A

acute lung injury leads to increase permeability that then causes increased lung water in the interstitial and alveoli now we have two issues: 1. reduced compliance
2. shunting (no ventilation but perfusion is present) leading to hypoxemia

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37
Q

wheen to administer PEEP?

A

when volume is low

38
Q

ventilator induced lung injury:

A
  1. volutrauma
  2. barotrauma
  3. biotrauma
  4. atelectrauma
39
Q

repetitive opening
and closing of alveoli can injury
alveoli

A

Atelectrauma:

40
Q

injury to lung
releases harmful cytokines 
further lung injury and injury
to other organs

A

Biotrauma:

41
Q

rupture of alveoli
with gas escaping into pleural
space (pneumothorax)

A

Barotrauma

42
Q

injury to lung

indistinguishable from ARDS

A

Volutrauma:

43
Q

PEEP keeps

A

alveoli open at end expiration

44
Q

what does cAMP does?

A

increase smooth muscle relaxation and thus bronchodilate

45
Q

Beta receptor for the lungs

A

Beta-2

46
Q

Beta-1 will do what?

A

increase heart rate and contractility

47
Q

who converts ATP to cAMP?

A

adenylate cyclase

48
Q

Tachycardia will be caused

A

Beta-1 stimulation due to some oral absorption or swallowing

49
Q

tremors with Beta-agonist?

A

Beta-2 fault

50
Q

albuterol

A

fast/ short acting

51
Q

slameterol

A

long acting

52
Q

black box warning for the long-acting beta agonist

A

regular use may increase risk of severe asthma episodes

53
Q

preferred asthma medications

A

inhaled corticosteroids

54
Q

cortisol has an efffect on

A

glucose metabolism due to the overlap in aldosterone thus there might be some problems with fat deposition

55
Q

breaks down muscle; catabolic effect

A

prednisone

56
Q

dexamethasone has only what type of activity

A

glutocorticoid leading to higher anti-inflammatory effects

57
Q

Acetylcholine will bind to muscarinic receptors leading to

A

bronchoconstriction

58
Q

ipratropium is a

A

muscarininc antagonist that prevents the release in cGMP thus reduced bronchoconstriction

59
Q

COPD does the best with which pharmacological tx.

A

muscarininc antagonistic long actign

60
Q

side-eefects of muscarinic antagonist

A

dry mouth, gut issues

61
Q

cromolyn

A

mast cell stabilizers

62
Q

theophylline

A

both a bronchodilator and an antgonist for bronchoconstriction

63
Q

Ipratropium

is short or long acting

A

short acting

64
Q

Tiotropium

short or long acting

A

long

65
Q

Indication for chronic O2 therapy:

A

PaO2 < 55 mmHg (<60 mmHg if Pulm HTN)

66
Q

a consequence of expiratory flow limitation

A

hyperinflation

67
Q

why is hyperinlfation bad for inspiration?

good expiration?

A

-Bad: diaphragm flat and fibers are shortened; elastic WOB increased

Good: higher lung volume maximizes elastic recoil; airways are wider at higher lung volumes

68
Q

Serum to pleural fluid albumin gradient < 1.2 g/dL

A

exudate

69
Q

hypoalbuminemia

A

nephrotic syndrome

70
Q

hemothorax treatment

A
  • requires chest tube drainage
71
Q

tension pneumothorax depends on

A

Degree of collapse depends on size of PTX and elasticity of lung.

72
Q

treatment for Pneumothorax

A

big pneumothorax gets a chest tube

small/minimal- 100%O2

73
Q

If PCWP > 15 mmHg

A

Pulm. venous HTN

74
Q

PCWP < 15 mmHg

A

PAH

75
Q

PH mean PA should be

A

more than 25 mmHg at rest

76
Q

General measure of PH tx.

A

oxygen and diuretics

77
Q

WHO group 1 tx for PH

A
  • calcium channel blockers
  • prostacyclins
  • endothelian antagonist
  • PD5-% antagonist
78
Q

PDE-5

A

blocks the production of cGMP

79
Q

Prostanglandins

A

promote adenylate cyclase

80
Q

PE can cause Pulm HT

A

true there is a release of mediators- seotonin

81
Q

V/Q perfusion is good for those that

A

had recurrent PE

82
Q

people dying of a PE

A

give a thrombolyisis

83
Q

How long to treat PE therapy?

A

depends on underlying cause

84
Q

Central, cavitates, obstructs airways
Hypercalcemia from ectopic PTH-like (Paraneoplastic)
Local spread is a big problem

A

squamous cells

85
Q

Most cases from tobacco
When lung cancer occurs in a patient without tobacco exposure it is usually Adenocarcinoma
Usu peripheral, generally don’t cavitate, can be slow growing
Metastases a big problem
Targeted therapy (EGFR, ALK, ROS-a)

A

adenocarcinoma

86
Q

slow-growing; mimics pneumonia

A

adenocarcinoma in situ

87
Q

ptosis, miosis, anhydoris, endophtalmus

A

horner’s syndrom

88
Q

ulnar radiation

A

pancoast/superior sulcus tumor

89
Q

facial and upper chest edema, suffusion of mucous membranes, plethora (vascular obstruction of SVC

A

SVC syndrome

90
Q

which cancer molecular analysis of tumor can result in targeted therapy that will improve response rate

A

adenocarcinoma

Pulmonology (13 decks)

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