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respiratory Flashcards

1
Q

etiology of asthma

A 
complex trait
genetic and enviro factors
hypersensitivity to stimuli 
-allergies
-a/w irritants 
-exercise
-strong odours 
-cold air
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2
Q

what is asthma?

A

reversible episodes of airway obstruction due to
•inflammation
•muscle hyperactivity (muscle in the wall of airway spasm)
chronic inflammation of airway persistent (longer the inflm the more damage)
•hyper-responsive a/w (irritants)
•recurrent, reversible bronchi spasm
other allergic disorders eg hay fever

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3
Q

what is the patho of asthma

A

trigger -> hypersensitivity ->2 phase response

acute and late phase

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4
Q

do you need prior sensitization to the allergen?

A

yes (type 1 HS)

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5
Q

acute phase response?

A

prior sensitization to allergen (type 1H)

subsequent exposure -> allergen binds to igE coated mast cells -> mediator release-> inflm

  • intercellular junctions open->allergens enter sub mucosa
  • Inc permb and mucus secretion-> edema of airways
  • PNS stimulated bronchospasm
  • a/w constriction (compensatory)

lasts up to 1hr

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6
Q

how long is the acute phas

A

up to 1 hour

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7
Q

when you breath in smoke (for example) what do your airways do to compensate? what phase?

A

constrict

acute

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8
Q

how long is the late acute phase

A

4-8 hours peak

can last up to weeks

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9
Q

what happens in late phase response

A

manifestations of acute phase persist

self sustaining cycle of exacerbation

influx of inflm cells

  • epithelial damage
  • fed mucociliary function bc mucus and exudate and overwhelmed cilia
  • hyper responsive airway bc inflm
    • respond to new triggers
    • frequent and severe episodes
  • inflm damage not healed and becomes accumulative

bronchoconstriction via a adrenergic receptors
bronchodilation via b adrenergic receipts
cAMP mediated and brings constriction/dilation when needed

lack of b receptor adrenergic stimulation??

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10
Q

what is the effect of mucus in terms of IR

A

overwhelms the cilia and bacteria like to grow here

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11
Q

when you bind a1 what does it do

A

constriction

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12
Q

what happens when you bind b1

A

dilation

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13
Q

manifestations of asthma

A 
dyspnea 
wheezing 
immobilization ??
bronchospasm & coughing 
Inc resp effort 
ventilatory compromise (alt resp status & ABGs)
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14
Q

DX of asthma

A

hx and px
labs
pulmonary function tests
inhalation challenge tests (because type 1: need allergen so this will show by applying allergen (inhale) to detect it)

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15
Q

asthma tx??

preventative ?

drugs?

A

prevent: avoid allergens & irritants
no smoking
drugs
step 1: inhaled short acting bronchodilators prn
(beta adrenergic)

step 2: add inhaled steroid
step 3: add long acting bronchodilator to steroid

step 4:

  • short course steroid
  • add 3rd drug -leukotriene receptor antagonist or theophylline
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16
Q

what is atelectasis

A

collapse of part of lung -impedes filling

affected part non fx

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17
Q

3 types of atelectasis

A

1) obstructive/resorption atelectasis
- a/w obstr (eg mucus) ->air trapped -> absorbed into capillaries -> local collapse

2) compression collapse
- ext pressure on lungs (eg by Tumor)

3) contraction atelectasis
- scar tissue contraction -> lung collapse

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18
Q

manifestations of atelectasis

A

dyspnea
tachypnea (trying to get more air in)
Dec chest expansion
tachycardia (comp) r/t delivery of o2 -> compromised gas exchange

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19
Q

atelectasis Dx

tx?

A

Px
CXR
CT
bronchoscopy

cause

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20
Q

what is a pleural effusion

A

fluid accumulation isn pleural space
d/t abnormal seepage +/or drainage
•exudate:inflm fluid, inc protein content
•transudate: non-inflm, dec protein content
•empyema: purulent (bact)
•hemothorax: blood
•chylothorax: lymph

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21
Q

et of pleural effusion

A

usually CHF
infect,
CA-> Tumor ->injury-> inflm->exudate
pulm infarct : obstr to blood flow (more push pressure)

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22
Q

patho of pleural effusion

A

fluid enters via parietal caps
drains into parietal lymphatics
fluid entry exceeds drainage

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23
Q

manifestations of plural effusion

A

based on cause and volume
•dyspnea
•pleuritic pain
•lung compression

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24
Q

pleural effusion Dx

A

X-RAY
CT
US

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25
pleural effusion Tx
cause thoracentesis (+ fluid analysis) chest tube
26
why don't you use volume expanded for the thoracentesis
not enough fluid
27
what is pulmonary edema
fluid accumulation in the alveoli pulmonary congestion in the vessel when blood volume increases drives Inc HP fluid in the lungs. Alveoli always lined with fluid so there's always fluid but this is accumulation
28
Et of pulmonary edema (pulmonary vascular disorders)
usually LHF •noncardiogenic: - IV fluid overload -smoke inhalation (fire: toxic fumes bring inflm -> alter permeability -> fluid into alveoli -aspiration -IV drug abuse (recreational) bc Inc permeability, depresses CNS -> controls resp and circulation
29
patho of pulmonary edema
fluid from blood to IS to alveoli --- dec resp function
30
Mnfts of pulmonary edema
cough -> productive (frothy bc air and fluid, blood tinged bc damage to vessel) dyspnea dec compliance crackles
31
Tx of pulmonary edema
resp support cause Inc heart function
32
what is a pulmonary embolism
clot that arises in the pulmonary circuit thrombus in pulmonary vessel (artery) usually develops from deep vein
33
is a pulmonary embolus in a vein or an artery
Artery
34
what is the recurrence rate of PE (%)
10% potentially lethal
35
et of pulmonary embolism
usually DVT (iliac, femoral, popliteal) other emboli •fat embolus bone marrow (if you fracture, the blood vessels in the marrow will be severed and fat will get into circulation) •air through IV •amnionic fluid -during birth, membranes rupture and fluid is released and blood vessels are severed in labour and sometimes matter in fluid enter the circulation and go through and cause PE
36
Patho of PE
DVT -> embolus -> thrombus in arterial bed-> impaired perfusion ventilation: perfusion imbalanced -> hypoxemia-> platelets degranulate-> bronchial and pulmonary artery constriction-> hemodynamic instability (blood vol, pressure, and flow) reflexive bronchoconstriction (sympathetic NS) conseq of what's going on dec CO l/o surfactant-> atlectasis RHF
37
PE where do the platelets come from? what do they do?
come through to release mediators (first obstruction, worsening -> ventilation is now impaired)
38
PE is ventilation or perfusion impaired
both. perfusion because of the embolus and ventilation because the platelets will release mediators that cause bronchial constriction too (and pulmonary artery constriction)
39
PE Why is there dec Co?
blood coming Into the pulmonary circuit from the right side of the heart but not enough going in so won't have enough to the left side
40
PE Why is there l/o surfactant
any secretion in the body requires some fluid and perfusion and the problem with perfusion cause ischemia and tissue damage
41
PE Why is RHF? will this cause LHF
obstruction of pulmonary circuit so right ventricle keeps pumping against Inc resistance and hyper trophy and would fail no
42
PE Mnfts
based on size and site -embolus varies in size and depending on the size different vessels will be affected usually - chest pain (ischemia), tachypnea, dyspnea - tachycardia
43
PE DX
hx and px ABGs -hypoxemia, hypercapnia, acid-base imbalance LDH3 lung scan (131 HSA, IV) CXR CT pulmonary angiogram
44
what does LDH3 measure
serum marker: lactate dehydrogenase (High conc in lung tissue) released when damage to tissue bc ischemia -> infarction
45
what does the lung scan measure
human serum albumin (protein present in serum) this can be synthesized. it is taken and labeled with iodine : these are radioisotopestag compounds tag that is going throughout the system. stop at he obstruction and you can see movement t in a screen. precise and not Invasive
46
PE Tx
stat tax anticoagulants and thrombolytics maintain cardiopulmonary fx address DVT
47
what is the pressure in pulmonary htn? what is the normal?
>25 mmHg and normal is 15
48
is there high pressure and high resistance in the pulmonary circuit or low?
low
49
if CO Inc, what happens to the pulmonary pressure?
minimal increase
50
if there is pulmonary vasoconstriction, what happens to the pressure of the pulmonary circuit
Inc
51
etiology of Pulmonary htn?
2° to cardiac and pulmonary problems 3 categories: 1) Inc pulmonary volume in arterial part (cardiac septal defect) 2) hypoxemia (normally vasodilation occurs but in the lungs it constricts and less blood leaves the pulmonary circuit and take on Co2 -> Inc pressure 3) Inc pulmonary venous pressure: left sided heart failure
52
manifestations of pulmonary htn
* dyspnea * syncope- usually d/t def of blood and o2 in the brain * chest pain in exertion * those of RSHF: abdominal distension, ascites * CXR: RV hyper trophy, distended pulm arteries * fatigue
53
Pulmonary htn Tx
cause vasodilators (could bring about systemic vasodilation) dec prognosis if severe
54
what is acute respiratory distress syndrome ? (ARDS) what is the mortality
severe damage to alveolar and capillary walls -acute onset, progressive 40-60% mortality
55
etiology of ARDS
``` aspiration (gastric content, HCL) Inc smoke inhalation drowning drugs (cocaine, heroin) fat embolus septicaemia ```
56
patho of ARDS
lung trauma -> neutrophil influx -> free radicals, phospholipids + proteases -> endothelial and alveolar damage -> Inc permeability -> effluent of proteins, cells, & fluids into IS and alveoli -> edema -> dec compliance and impaired gas exchange profound hypoxemia
57
what is inactivated in patho of ARDS what follows
surfactant def and inactivation-> leads to atelectasis
58
what forms around the alveoli in ARDS
thick protein and cell exudate lines alveoli impervious hyaline membrane
59
mnfts of ARDS
``` acute onset resp distress dyspnea (early sign) tachypnea hypoxemia early resp alkalosis late metb acidosis diffuse consolidation ```
60
ARDS TX
early intervention reverse cause resp support complications
61
what kinds of tumours cause lung cancer
primary and secondary develops in the lung (primary) also received metastatic tumors from elsewhere (secondary)
62
characteristics of lung cancer ? mortality rate ? (fraction)
aggressive, invasive, metastatic 1/3
63
where does lung cancer spread
bone liver and brain
64
what are the 4 major types of lung cancer
adenocarcinoma (30% squamous cell carcinoma (30%) large cell carcinoma (12%) small cell carcinoma (22%) first 3 are NSCLC last is SCLC
65
et of lung cancer
smoking >80% genetic predisposition toxins (asbestos)
66
patho of squamous cell carcinoma
arises in central bronchi (hilum) spreads to hilar nodes more common in men
67
adenocarcinoma patho
peripheral origin alveoli Of bronchioles common in woman and non smokers
68
large cell carcinoma
peripheral origin (bronchioles of alveoli) Tumor is large undifferentiated cell early metastasized poor prognosis
69
small cell carcinoma patho
``` 99% smokers aggressive, invasive and early metast (esp brain) •worst form •small oval cells •mets at Dx •non resectable •radio sensitive •paraneoplastic syndrome (SIDAH, crushings) ```
70
mnfts of lung cancer
``` based on: type, site extent paraneoplastic syndrome •if central -> impairs ventilation -> coughing, wheezing, dyspnea (bronchi and a/w) •Hemoptysis (damaged blood vessels from Tumor ) •pain •cardiac mnfts ```
71
lung cancer Dx
hx, px CXR, US CT MRI bronchoscopy - collect a biopsy, needle biopsy cytology (sputum or bronchial wash) to identify the bronchial types
72
lung cancer tx
NSCLC: sx, radiation and chemo SCLC: chemo and radiation
73
where in the body can you get cystic fibrosis?
anywhere that has exocrine glands
74
what is cystic fibrosis
defective cl channels in cell membrane hypersecretion of mucus in resp and pancreas would be pancreatic juices and a change of the characteristic of the secretion leads to hypersec of fluid in GIT, reprod, and resp system
75
et of cystic fibrosis
CFTR gene on chr 7 (cystic fibrosis transmembrane regulator protein/gene) Autosomal recessive
76
patho of cystic fibrosis
look at diagram. basically if you have Inc cl in cell wall inc concentration so water will want to follow and sodium will follow and now mucus has nothing and gets sticky, thick ``` CFTR forms cl channels on epith cells mutation makes cell inlets me to cl impaired cl transport across membrane Abn sticky mucus ideal for bact growth and ventilation is impaired and mucociliary blanket is defective in moving the mucus ``` thick mucus -> dec ciliary fx-> plugs airway -> dec fx >90% will die with severe pulm disease
77
cystic fibrosis Dx
sweat test measure NaCl in perspiration be this is 2-5x higher in cystic fibrosis CF in sibling newborn screen (trypsinogen) --- precursor for trypsin and is elevated in infant blood bc obstr jn duct of pancreas and those secretions move in the blood GI tract mnfts and resp mnfts
78
TX of cystic fibrosis
no cure DNAase (Dec. mucus stickiness) breaks down DNA but not destr in intact cells. destroys DNA in mucus from damaged cells. makes the mucus less stringy and can expectorate it more easily control infect diet modification and pancreatic E supplement antiinflm gamma globulins for IR
79
what is resp failure
lungs fail to function no gaseous exchange -- hypercapnia and hypoxemia
80
cause of resp failure ?
``` COPD pneumonia atelectasis tumors Gillian barre pulmonary edema ARDS ```
81
what are mnfts of resp failure
hypoxemia PaO2 45 | resp acidosis
82
tx of resp failure
``` restore gas exchange 02 mechanical ventilation bronchodilation abx ```

patho (12 decks)

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