PM Asthma, atelectasis, pleural effusion Flashcards

1
Q

what is chronic about asthma

A

chronic inflm of the airway
the airways is hyper-responsive
there are recurrent, reversible bronchospasm
(it is chronic but it has episodes)

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2
Q

what is reversible about asthma

A

asthma has reversible episodes of airway obstruction that is due to

  • inflm
  • muscle hyperactivity (of the airway->spasm)
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3
Q

asthma is?? also? other than reverisble episodes of a/w obstr and chronic inflm of the a/w

A

other allergic disorders

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4
Q

et of asthma

A
  • complex trait
  • genetic and enviro factors
  • hypersensitivity to stimuli (these are triggers)
    • allergens
    • a/w irritants
    • exercise
    • strong odours
    • cold air
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5
Q

fig 29.6

A

d

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6
Q

fig 29.6

A

f

fi

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7
Q

fig 29.6

A

f

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8
Q

differences in time of early vs late phase in relation to timing

A

early phase peaks in 5min

late phase is more progressive and can last months

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9
Q

why does the late phase last so long

A

there is a cyclic inflm that attracts more inflm cells etc.

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10
Q

does the early or late phase have mucus

A

late

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11
Q

what is necessary for the acute phase response to occur

A

prior sensitization to allergen (TYpe 1 hypersensitivyt0

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12
Q

what happens acute phase after subseq exposure

A

allergen binds to IgE coated mast cells->mediator release->inflm

  • intercellular junction open->allergens enter submucosa
  • inc permb and increased mucus secretion->edema of the airways
  • PNS stimulated to bronchospasm
  • dyspnea and wheezing
  • a/w constriction (compensatory)
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13
Q

is the bronchospasm from PNS beneficial in the acute phase of asthma

A

no

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14
Q

how long does acute phase last

what could alter this

A

up to 1hr (unless they take their meds to stop/prevent it

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15
Q

how is the a/w constriction compensatory that occurs in acute phase response

A

eg in inhale smoke or irritant the a/w contricts to limit amount of irritant that gets in. the a/w constriction will further irritate the asthma)

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16
Q

why does wheezing sound the way it does

A

blowing through a narrow tube

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17
Q

what occurs in the late phase response of asthma
peak
what type of mnfts do you see

A

peaks in 4-8hrs

mnfts (dyspnea, wheezing, edema of a/w, a/w constriction persist)

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18
Q

what occurs in the late phase response of asthma

A
self sustaining cycle of exacerbation
can last days to weeks
-there is influx of inflm cells (basophils, eosinophils etc)
   -epithelial damage
   -dec mucociliary fx
   -hyperresponsive a/w 
      -respond to new triggers (eg cold air)
       -freq and severe episodes
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19
Q

why is the a/w hyperresponsive in late phase of asthma

A

d/t inflm change

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20
Q

do recurrent attacks get better o worse

A

they get worse d/t cumulative damage

there are EPISODES they are NOT periods of exacerbation and remission

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21
Q

which receptors cause broncho contriction and dilation

A

alpha adrenergic receptors cause bronchoconstriction

beta adrenergic receptors cause bronchodilation

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22
Q

what mediates the broncho/contr/dilation

A

cAMP (a second messenger)

23
Q

what might be lacking in asthma

A

a lack of beta receptor stimulation in asthma??

24
Q

mnfts of asthma

A

-dyspnea
-wheezing
-immobilization
-bronchospasm
-coughing
-inc resp effort
-ventilatory compromise–alt resp status and ABGs (youll see hypoxemia, changes in pH, acidosis, hypercapnia
DWIB VIC the dweeb who lives in Vic

25
Q

dx of asthma

what are they trying to separate it from?

A

(they are trying to separate it from respiratory tract infection)
hx, px
labs
pulm fx tests (these will show alt resp status)
inhalation challenge tests (we need alllergen because it is a T1H. this is like an allergy test. IF hyperresponsive they have asthma

26
Q

tx of asthma

A

control w preventative meds

27
Q

what are preventative measures for asthma

A

avoid allergens and irritants

no smoking

28
Q

durgs for asthma
at what level is it usually enough?
steps 1-4

A

step 1: inhaled short acting (beta) bronchodilators PRN
step 2: add inhaled steroids (these first two steps are generally enough for eveyrone)
step 3 add lng acting bronchodilator to the steroid
step 4: short course oral steroid
ass 3rd drug-leukotriene receptor antagonist or theophylline

29
Q

fx of leukotriene receptor antagonist

A

(blocks inflm and Type 1 H)

30
Q

theophylline fx

A

bronchodilator w anti inflm effects

31
Q

what are the disorders of lung inflation?

A

atelectasis

, pleural effusion. maybe more?

32
Q

what is atelectasis

A

collapse of part of lung->impedes filling (this is usually only a small part of the lung, surfactant prevents the sides from sticking together)
-affected part is non functional

33
Q

types of atelectasis

A

obstructive resporptive
compression atelectasis
contraction atelectasis

34
Q

obstr/resorptive atelectasis

A

-a/w obstr eg by mucus)->air trapped (distal to obstr)->absorbed into capillaries->lung collapse

35
Q

compression atelectasis

A

external pressure on lungs eg by tumor

36
Q

contraction atelectasis

A

scar tissue contraction ->lung collapse

37
Q

mnfts of atelectasis

A
  • dyspnea
  • tachypnea (to get more O2)
  • dec chest expansion
  • tachycardia (compensatory)
38
Q

is atelectasis reversible

A

if not in place too long you can fix it

39
Q

dx of atelectasis

A

px
CXR
CT
bronchoscopy

40
Q

fig 29.4

A

r

41
Q

tx of atelectasis

A

cuase

42
Q

pleural effusion aka

A

hydrothorax

43
Q

what is pleural effusion

A

fluid accum in pleural space (betweent he pleural membranes)

  • d/t abn seepage and or drainage
    • exudate: inflm fluid, inc protein content
    • transudate: non inflm fluid, dec protein content
44
Q

pleural effusion of lymph aka

A

chylothorax

45
Q

pleural effusion of blood aka

A

-hemothorax: blood

46
Q

pleural effusion of pus

A

-empyema: purulent

47
Q

et of pleural effuson

A

usually CHF (L sided is lung and R sided is rest of body)
-infection
CA (tumor in pulm system)
pulmonary infarction. (infarction->dec blood flow->inc push pressure->hydrothorax)

48
Q

dx of pleural effusion

A

xray (might not give enough info)
US
CT

49
Q

tx of pleural effusion

A

cause
-thoracentesis and fluid analysis
chest tube (this and thoracentesis wont work if the pus solidifies or blood coagulates. youd have to do sx)

50
Q

can pleural effusion be deadly

A

yes with large volume

51
Q

what is given to some palliative care pts and repeticie cases

A

sclerosing agents that causes the lungs to stick together and fluid cant get in

52
Q

What causes the airway obstruction that reversible?

A

Inflation and muscle hyperactivity(muscle spasm)

53
Q

What causes the chronic inflammation of the airway in asthma

A

The airway is hyper responsive

There is recurrent reversible bronchi spasm (recurrent due to triggers)