respiratory review Flashcards

1
Q
if sputum is 
green / yellow
rusty
thick / copius 
hemoptysis
A

green / yellow –> some infection
rusty –> pneumococcal penumonia infection
thick / copius –> CF, asthma, bronchitis
hemoptysis –> full RBC’s in blood

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2
Q

what are expectorants? e.g. guaifensesin

A

drugs used to make secretions more watery

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3
Q

breathing: what is kussmaul?

A

Kussmaul –> rapid, deep breathing usually caused by acidosis (need to get rid of CO2) from diabetes

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4
Q

breathing: what is Cheyne-Stokes?

A

periodic breathing with apnea caused by brain damage

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5
Q

t or f, dyspnea is a perception of difficult inspiration but actually effects expiration

A

true

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6
Q

wheezing
stridor
rales
Ronchi

A

wheezing - lower airways
stridor - upper airways, crowing noise
rales - crackling noise from secretions
Ronchi - deep noise from thick mucus

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7
Q

t or f, CO2 is less soluble and diffuses slower than O2

A

false - CO2 diffuses faster - less affected when there are perfusion issues

get rid of CO2 fast but don’t take in O2 - alkalosis?

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8
Q

what is emphysema?

A

COPD caused by trypsin related destruction of alveoli walls.
deficiency in anit-trypsin (liver) –> caused by smoking or by congenital reasons.

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9
Q

t or f
emphysema
increase lung compliance
decreased lung recoil (increased radii)
decreases surface area - problem with perfusion
decreases vasculature - V/Q mismatch
decreases interdependence between alveoli

A

true

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10
Q

why does emphysema cause obstruction?

A

lower airways are thin
there is lack of recoil
requires increased pleural pressure to expel air which causes airway collapse and expiratory problems

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11
Q

what is hyperinflation?

A

air trapping –> cannot expel air –> patients become barrel chested due to increased thoracic size

the diaphragm also remains flat at rest (normally its flat during inspiration) –> opens more space for air

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12
Q

what are bullae?

A

super-alveioli formed in emphysema

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13
Q
how are the following affected in emphysema
TLC
VC
IRV
RV
FEV1
ERV
A
TLC - increased (hyperinflation)
VC - decreased (less air exchange)
IRV - decreased since air is trapped - blocks new air
RV - increased since air is trapped
FEV1 - decreased - below 70% of FVC
ERV - decreased
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14
Q

if there is increased lung recoil and we breath in with high tidal volume what occurs?

if there is increased airway resistance (decreased radius) and we breath with high frequency what occurs?

A

both situations increase work

high resistance - should combat with tidal volume

high recoil - should combat with frequency

we normally breathe with high Tv and lower frequency –> decreases % of air in dead space

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15
Q

t or f, in emphysema, the work for inspiration is easier than normal

A

true –> no recoil = easy to breathe in…

but expiration is very difficult

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16
Q

tachycardia
tripod position
pursed lips

compensations of emphysema, explain.

A

tachycardia –> increases blood flow to lungs
tripod position –> engages pectoral muscles in respiration
pursed lips –> increases airway pressure - avoids airway collapse

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17
Q

during middle stage emphysema, there is a V/Q mismatch - what is this?

A

ventilation is still high but since their is destruction of so many capillaries, there is poor blood flow and many unperfused area’s which do not take up the available oxygen.

wasted ventilation

18
Q

what occurs in the lungs when air is not being perfused into capillaries?

A

vasoconstriction - areas where oxygen uptake is difficult will stop receiving blood

body is trying to redirect blood to O2 rich areas

19
Q

what is a major consequence of late stage emphysema –> cor pulmonale –> what is this?

A

Enough area now has poor perfusion –> vasoconstriction occurs everywhere –> increases pulmonary pressure which backs up onto the right heart and causes right heart failure

20
Q

t or f, middle stage emphysema - hypocapnia

late stage emphysema - hypercapnia

A

true

middle stage –> you hyperventilate. since CO2 diffuses faster than O2, you get rid of more CO2 then take in O2 –> acidosis

late stage –> your compensatory measures fail - so hard to expire that CO2 builds up and causes hypercapnia

21
Q

what is the hypoxic drive? what controls respiration?

A

normally CO2 levels are detected in the medulla and control respiration –> when the CO2 levels are low the hypoxic drive may kick in –> carotid artery O2 receptors take control of respiration if O2 mmHg drop below 60.

22
Q

why can’t you give someone oxygen therapy who has PaO2 above 60 mmHg?

A

then the body perceives that you have enough oxygen and slows respiration –> but CO2 levels are still building up –> acidosis

23
Q

what is chronic bronchitis (3)

A
  • goblet cell hyperplasia - mucosal secretions
  • mucosal edema
  • fibrosis from chronic inflammation

all cause obstruction

24
Q

what breathing sound does bronchitis make?

A

Ronchi - deep due to mucus

emphysema makes wheezing sound

25
Q

can bronchitis cause cor pulmonale?

A

yes –> chronic cough increases pulmonary HT –> RHF

26
Q

t or f, in emphysema, cyanosis occurs faster than in bronchitis

A

false - bronchitis occurs faster

emphysema is slower since there is more compensation for the disease

27
Q

what airways does asthma effect?

A

airways large enough to have smooth muscle

28
Q

what is extrinsic asthma?
other name?
mechanism? late vs early rxn?

A

extrinsic asthma is a type 1 IgE mediated hypersensitivity reaction (allergy) responding to some allergen.

think Extrinsic = A(e)llergy

its also called atopic asthma since it is an inheritable allergy

  1. IgE binds allergen –> degranulation of mast cell, histamine, kinin –> bronchoconstriction, edema, decreased HR
  2. late stage –> recruited eosinophils release leukotrienes –> exacerbates inflammation. ROS may cause epithelial damage.
29
Q

what is intrinsic asthma?
other name?
mechanism? late vs early rxn?

A

non-atopic asthma
caused by unknown irritant –> cold air, smoke, aspirin (enhances leukotriene pathway)
IgE mediated and Th cell mediated (type 4 HS?)

intrinsic asthma –> NOT allergic –> negative skin prick test

think: no known allergy - cause must be intrinsic to you

30
Q

t or f, asthma causes a decrease in peak expiratory flow and a decrease in FEV1 relative to VC (i.e. FEV1 drops more than VC)

A

true

31
Q

what is pulses paradoxes

A

indicates more effort to inspire due to increased (-) pleural pressure which causes greater than a 10mmHg drop in pulse pressure during inspiration

later effect of asthma

32
Q

after time, what occurs to the airways in asthma?

A

airway remodelling –> becomes thicker, with more SMC’s, fibrosis –> overall harder to breath though

33
Q

status asthmaticus?

A

persistent asthma attacks despite treatments

34
Q

does asthma produce a productive cough?

A

yes

35
Q

t or f, there are 2 general causes of restrictive disease

  1. muscle compromise - MG, MD, etc.
  2. interstitial fibrosis
    - irritant
    - microbe
    - idiopathic
A

true

36
Q

In interstitial fibrosis, what causes the CRPD?

A

persistent irritation does not allow apoptosis of fibroblasts –> their prolonged activation lays down too much scar tissue –> restricts lung expansion

37
Q

what occurs to FEV1 in restrictive disorders?

A

unlike asthma where FEV1 drops by more than VC,

FEV1 drops proportionally to VC in restrictive disorders

38
Q

is there a problem with expiration in restrictive disorders?

A

yes - less expansion = less recoil too, so it is somewhat affected

39
Q

pulmonary fibrosis is?
why does it have a low V/Q?
what levels of O2 and CO2 does it cause?

A

pulmonary fibrosis is scarring of the interstitial space in lungs.
low V/Q b/c fibrosis hinders perfusion –> low effective ventilation for the amount of blood flow (opposite to emphysema)
hypoxemia due to low inspiration
hypercapnia - ?? not sure y, just know

40
Q

what is pneumoconiosis

A

pneumoconiosis is pulmonary fibrosis due to prolonged exposure to an irritant

41
Q

does pneumoconiosis cause mesothelioma (cancer of pulmonary membranes)?

A

if the irritant is an asbestosis (to do with certain minerals), it may cause mesothelioma. this in turn may cause pleural effusion and pneumothorax (atelectasis)