Respiratory Flashcards

(51 cards)

1
Q

Oxygenation of Hb promotes dissociation of H+ from Hb, this shifts equilibrium toward CO2 formation;therefore, CO2 is released from RBCs

A

Haldane effect

  • in the lung
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2
Q

Increase in H+ from tissue metabolism shifts curve to righ,unloading O2.

A

Bohr effect

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3
Q

interdifitating ares of pink(platelets) and red(RBCs) found ONLY IN THROMBI FORMED BEFORE DEAD

A

LINES OF ZAHN

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4
Q

↓↓FEV/↓FVC<80%

↑RV

V/Q mismatch

A

Obstructive lung diseases

  • chronic bronchitis
    • blue bloater
  • emphysema
    • pink puffer
  • Asthma
  • bronchiectasia
  • lead pulmanry hypertention(>25mmHg)and finally to corp pulmonale (decrease in O2 casues pulmonar vasoconstrctition)
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5
Q

Ththickness of gland layer/total thickness of bronchial wall>50%

A

Reid index

  • greater tahn 50% in chronic bronchitis
  • productive cough for >3 months per year for > 2 years.
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6
Q

dysnea,cough ,minim sputum and purse libs exalation

A

Emphysema

  • exalation through pursed lips to increase airway pressure and prevent airway collapse during respiration.
  • decrease lung recoil, increase compliance resulting from destruction of alveolar walls
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7
Q

ration of the pulmonary artery yo the blonchus at each lung hilus is described by?

A

RALS

right anterior

left superior

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8
Q

aspirate peanut:

while upright

while supine

A
  • while upright:lower portion of right inferior lobe
  • while supine:superior portion of right inferior lobe
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9
Q

structures perforatin diaphragm

at T8

at T10

at T12

A

I (IVC) ate(8) ten(10) eggs(esophagus) at(aorta) twelve(12)

at T8=IVC

at T10=esophagus,vagus

at T12=aorta,thoracic duct,azygos veins

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10
Q

air that can still be breathed in after normla inspiration

A

inspiratory reserve volume

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11
Q

air can still be breathed out after normal expiration

A

Expiratory reserve volume

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12
Q

Air in the lungs after maximal expiration

A

Residual volume

  • cannot be mesure by spirometry
  • incrased in obstructive lung disease
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13
Q

Determination of pysiologic dead space:anatomic dead space +functional dead space in alveoli.

A

VD=VT*PaCO2-PECO2/PaCO2

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14
Q

total volume of gas entering the lungs per minute

A

MINUTE VENTILATION(VE)

VE=VT*RR(respiratoy rate)

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15
Q

volumen of gas per unit of time that reaches the alveoli

A

Alveolar ventilation(VA)

VA=(VT-VD)*RR

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16
Q

Tau HB

Relaxed Hb

A
  • Tau in Tissue has low affinity to O2 leading to increase O2 unloading(curv to the right)
    • CL,H+,Co2 and temperature favor tau
  • Relaxed Hb high affinity for O2 in the respiratory tract
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17
Q

Methemoglobin treatment

A

Methylene blue

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18
Q

Whats Methemoglobyn

A

It is FERRIC Fe3+ hemoglobin that does not bing O2 readily, but has increase affinity for cyanide.

nitrates cause poisoning by oxidizing Fe+2 to Fe+3

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19
Q

Cyanide poisoning treatment(present in nitroprusside)

A

use nitrites to oxidaze Hb to methemoglobin,which binds cyanide.use thiosulfate to bind this cyanide,foming thiocyanate,which is renally excreted

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20
Q

cherry red skin and dead

A

CO posioning

  • carboxyhemoglobin shift curve to the left, decreasing unloading in tissues
  • normal pulsoxymeter
  • TX:100% O2
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21
Q

what does a decrese in PAO2 does to the pulmonary circulation?

A

↓ in PAO2 causes a hypoxic vasoconstriction

In an effort to shift blood away from poorly ventilated regions of the lung to well-ventilated regions of lung

22
Q

what does an increase in A-a gradient (normal 10-15) means

A

An incresea in A-a(>15) means Hypoxemia

  • shunting
  • V/Q mismatch
  • intertitial lung disease
23
Q

normal A-a gradient with hypoxemia(decreased PaO2)

A
  • hypoventilation
  • High altitude
24
Q

V/Q=0

A

Airway obstruction(shunt) in shunt 100% does nor improve PO2

25
V/Q=infinit
blood flow obstruction
26
body response to high altitude(↓PaO2)
**ACUTE** causes hyperventilation and respiratory alkalosis. **LATE** ↑erythropoietin ↑2,3BPG (shifh curve to re righ) ↑renal excretion of HCO3(can ve augment by use of acetazolamide) to compensate for the respiratory alkalosis
27
response to exercise by the lung
* V/Q from apex to base becomes uniform * no change on PaO2 and PaO2 * increase venous CO2 and decrese venous O2
28
virshow traid:
* stasis * hypercoagulability * Endothelial damage
29
Sudden onset dysnea,tachypnea,tachycardia, altered mental status, petechial rash.
**_Pulmonary Emboli_** * fat * air(gas) treat with hyperbaric oxygen Caisson´s disease * thrombous * bacteria * amniotic fluid * tumor
30
Curschmann spirals(shed epithelium forms mucus plugs) found in asthma
31
**_Charcot-Leyden crystals_** * formed from breakdown of eosinophils in sputum * found in asthma
32
cough ,foul-smelling sputum,dysnea
**_Bronchiectasis_** associated with bronchial obstruction * kartagener * cystif fibrosis * allergic bronchopulmonary aspergilosis
33
↓FEV/**↓↓**FVC\>80% ↓all lung volumes
**_Restrictive lung disease_** **Poor brething mechanics(normal A-a gradient)** * poor muscular effor-polio,myastenia gravis * poor structural apparatus-scoliosis,morbid obesity **Interstitial lung disease**(pulmonary decrese diffusing capacity,↑A-a gradient)
34
what does acute suplementary O2 ARDS patients can cause death?
in ARDS patientes respiration is driven by central CO2 concentration, an increase in O2 will decrease CO2 leading to respiratory supression and coma.
35
**_Ferruginous bodies_** * found in asbestosis related to bronchogenic carcinoma and mesothelioma, lower lung. * associated with shipbuilfing,roogin and plumbing.
36
eggshell calcification of hilar lymph nodes
**_Silicosis_** ## Footnote * foundries * sandblasting * mines * silica disrupt phagolysosomes and impari macrophages(susceptibility to TB) * increse risk of bronchogenic carcinoma
37
neonatal respiratoy syndrome risk factor and complications
Risk factors: * prematurity * maternal DM(due to feal increase in insulin, and insulin its an inhibitor of surfactant production dependent on steroids) Complications: * PDA * NEC * supplemental O2(free radical damage) * retinopathy * bronchopulmonar dysplasia
38
damage in BMPR2 with media hypertrophy
primary pulmonary hypertention
39
most common lung cancer in nonsmokesand overall
**adenocarcinoma** * Peripheral * K-ras,EGFR and ALK mutation * associated with clubbing
40
adenocarcinoma of the lung in situ
**_bronchiolovar subtype_** of the adenocarcinoma * CXR:hazy infiltrated similar to pneumonia * apparent thickenin of alveolar walls.
41
caitaiton , cigarret relate and hypercalcemia related lung cancer
**squamos cell carcinoma** ## Footnote produces PTHrP keratin pearls and intercelular bridges
42
lung cancer with these three paraneoplasic syndromes : ACTH ADH Lamber-Eaton
**_small cell(oat cell) carcinoma_** * central * amplified Myc * inoperable:treat with chemo * neuroendocrine neoplasm of kulchitsky cells-\>salt and paper aparience
43
less responsive to chemoteraphy lung cancer higly anaplastic
**_large cell carcinoma_** peropheral
44
chromogranin A possitive lung cancer
**_Bronchial carcinoid tumor_** not associated with cigarret
45
intertitial pneumonia in transplanted patients
CMV pneumonia * diffuse patchy inflammation localized to interstitial areas at alveolar walls. * indolent course.
46
**_Lung abscess_** air-fluid levels often seen on CXR oftehn due to S.aureus or anaerobes.
47
cuts S bound in mucus
N-acetylcysteine
48
induces bronchodiltation by increasing cAMP
**ß2 agonist** * Alburetol * long acting:salmeterol, formeterol
49
promotes bronchodilation by inhibitil PDE and decreasin hydrolysis os cAMP
Methylxantines * theophylline * blocks adenosine(adenosine cause bronchoconstriction)
50
preven bronchoconstriction by inhibitin M3 muscarinic receptors
**Muscarinic antagonis** * short acting:ipatropium * long acting:Tiotropium * used in ARDS
51