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patho > respiratory > Flashcards

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
Q

pleural effusion Tx

A

cause
thoracentesis (+ fluid analysis)
chest tube

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26
Q

why don’t you use volume expanded for the thoracentesis

A

not enough fluid

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27
Q

what is pulmonary edema

A

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

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28
Q

Et of pulmonary edema (pulmonary vascular disorders)

A

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

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29
Q

patho of pulmonary edema

A

fluid from blood to IS to alveoli — dec resp function

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30
Q

Mnfts of pulmonary edema

A

cough -> productive (frothy bc air and fluid, blood tinged bc damage to vessel)

dyspnea
dec compliance
crackles

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31
Q

Tx of pulmonary edema

A

resp support
cause
Inc heart function

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32
Q

what is a pulmonary embolism

A

clot that arises in the pulmonary circuit
thrombus in pulmonary vessel (artery)
usually develops from deep vein

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33
Q

is a pulmonary embolus in a vein or an artery

A

Artery

34
Q

what is the recurrence rate of PE (%)

A

10%

potentially lethal

35
Q

et of pulmonary embolism

A

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
Q

Patho of PE

A

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
Q

PE

where do the platelets come from? what do they do?

A

come through to release mediators (first obstruction, worsening -> ventilation is now impaired)

38
Q

PE

is ventilation or perfusion impaired

A

both. perfusion because of the embolus and ventilation because the platelets will release mediators that cause bronchial constriction too (and pulmonary artery constriction)

39
Q

PE

Why is there dec Co?

A

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
Q

PE

Why is there l/o surfactant

A

any secretion in the body requires some fluid and perfusion and the problem with perfusion cause ischemia and tissue damage

41
Q

PE

Why is RHF?

will this cause LHF

A

obstruction of pulmonary circuit so right ventricle keeps pumping against Inc resistance and hyper trophy and would fail

no

42
Q

PE

Mnfts

A

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
Q

PE

DX

A

hx and px
ABGs -hypoxemia, hypercapnia, acid-base imbalance

LDH3

lung scan (131 HSA, IV)
CXR
CT
pulmonary angiogram

44
Q

what does LDH3 measure

A

serum marker: lactate dehydrogenase (High conc in lung tissue) released when damage to tissue bc ischemia -> infarction

45
Q

what does the lung scan measure

A

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
Q

PE

Tx

A

stat tax

anticoagulants and thrombolytics

maintain cardiopulmonary fx

address DVT

47
Q

what is the pressure in pulmonary htn? what is the normal?

A

> 25 mmHg and normal is 15

48
Q

is there high pressure and high resistance in the pulmonary circuit or low?

A

low

49
Q

if CO Inc, what happens to the pulmonary pressure?

A

minimal increase

50
Q

if there is pulmonary vasoconstriction, what happens to the pressure of the pulmonary circuit

A

Inc

51
Q

etiology of Pulmonary htn?

A

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
Q

manifestations of pulmonary htn

A
  • 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
Q

Pulmonary htn Tx

A

cause
vasodilators (could bring about systemic vasodilation)
dec prognosis if severe

54
Q

what is acute respiratory distress syndrome ? (ARDS)

what is the mortality

A

severe damage to alveolar and capillary walls
-acute onset, progressive
40-60% mortality

55
Q

etiology of ARDS

A 
aspiration (gastric content, HCL)
Inc smoke inhalation
drowning
drugs (cocaine, heroin)
fat embolus 
septicaemia
56
Q

patho of ARDS

A

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
Q

what is inactivated in patho of ARDS

what follows

A

surfactant def and inactivation-> leads to atelectasis

58
Q

what forms around the alveoli in ARDS

A

thick protein and cell exudate lines alveoli

impervious hyaline membrane

59
Q

mnfts of ARDS

A 
acute onset resp distress 
dyspnea (early sign)
tachypnea 
hypoxemia 
early resp alkalosis 
late metb acidosis 
diffuse consolidation
60
Q

ARDS TX

A

early intervention
reverse cause
resp support
complications

61
Q

what kinds of tumours cause lung cancer

A

primary and secondary

develops in the lung (primary) also received metastatic tumors from elsewhere (secondary)

62
Q

characteristics of lung cancer ?

mortality rate ? (fraction)

A

aggressive, invasive, metastatic

1/3

63
Q

where does lung cancer spread

A

bone liver and brain

64
Q

what are the 4 major types of lung cancer

A

adenocarcinoma (30%
squamous cell carcinoma (30%)
large cell carcinoma (12%)
small cell carcinoma (22%)

first 3 are NSCLC
last is SCLC

65
Q

et of lung cancer

A

smoking >80%
genetic predisposition
toxins (asbestos)

66
Q

patho of squamous cell carcinoma

A

arises in central bronchi (hilum)
spreads to hilar nodes
more common in men

67
Q

adenocarcinoma patho

A

peripheral origin
alveoli Of bronchioles
common in woman and non smokers

68
Q

large cell carcinoma

A

peripheral origin (bronchioles of alveoli)
Tumor is large undifferentiated cell
early metastasized
poor prognosis

69
Q

small cell carcinoma patho

A 
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
Q

mnfts of lung cancer

A 
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
Q

lung cancer Dx

A

hx, px
CXR, US CT MRI
bronchoscopy - collect a biopsy, needle biopsy
cytology (sputum or bronchial wash) to identify the bronchial types

72
Q

lung cancer tx

A

NSCLC: sx, radiation and chemo
SCLC: chemo and radiation

73
Q

where in the body can you get cystic fibrosis?

A

anywhere that has exocrine glands

74
Q

what is cystic fibrosis

A

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
Q

et of cystic fibrosis

A

CFTR gene on chr 7 (cystic fibrosis transmembrane regulator protein/gene)

Autosomal recessive

76
Q

patho of cystic fibrosis

A

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
Q

cystic fibrosis Dx

A

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
Q

TX of cystic fibrosis

A

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
Q

what is resp failure

A

lungs fail to function
no gaseous exchange
– hypercapnia and hypoxemia

80
Q

cause of resp failure ?

A 
COPD
pneumonia 
atelectasis
tumors 
Gillian barre
pulmonary edema 
ARDS
81
Q

what are mnfts of resp failure

A

hypoxemia PaO2 45

resp acidosis

82
Q

tx of resp failure

A 
restore gas exchange
02
mechanical ventilation 
bronchodilation 
abx

patho (12 decks)

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