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my step1 > Respiratory > Flashcards

Respiratory Flashcards

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
Q

V/Q=infinit

A

blood flow obstruction

26
Q

body response to high altitude(↓PaO2)

A

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
Q

response to exercise by the lung

A
  • V/Q from apex to base becomes uniform
  • no change on PaO2 and PaO2
  • increase venous CO2 and decrese venous O2
28
Q

virshow traid:

A
  • stasis
  • hypercoagulability
  • Endothelial damage
29
Q

Sudden onset dysnea,tachypnea,tachycardia, altered mental status, petechial rash.

A

Pulmonary Emboli

  • fat
  • air(gas) treat with hyperbaric oxygen Caisson´s disease
  • thrombous
  • bacteria
  • amniotic fluid
  • tumor
30
Q
A

Curschmann spirals(shed epithelium forms mucus plugs)

found in asthma

31
Q
A

Charcot-Leyden crystals

  • formed from breakdown of eosinophils in sputum
  • found in asthma
32
Q

cough ,foul-smelling sputum,dysnea

A

Bronchiectasis

associated with bronchial obstruction

  • kartagener
  • cystif fibrosis
  • allergic bronchopulmonary aspergilosis
33
Q

↓FEV/↓↓FVC>80%

↓all lung volumes

A

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
Q

what does acute suplementary O2 ARDS patients can cause death?

A

in ARDS patientes respiration is driven by central CO2 concentration, an increase in O2 will decrease CO2 leading to respiratory supression and coma.

35
Q
A

Ferruginous bodies

  • found in asbestosis related to bronchogenic carcinoma and mesothelioma, lower lung.
  • associated with shipbuilfing,roogin and plumbing.
36
Q

eggshell calcification of hilar lymph nodes

A

Silicosis

  • foundries
  • sandblasting
  • mines
  • silica disrupt phagolysosomes and impari macrophages(susceptibility to TB)
  • increse risk of bronchogenic carcinoma
37
Q

neonatal respiratoy syndrome risk factor and complications

A

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
Q

damage in BMPR2 with media hypertrophy

A

primary pulmonary hypertention

39
Q

most common lung cancer in nonsmokesand overall

A

adenocarcinoma

  • Peripheral
  • K-ras,EGFR and ALK mutation
  • associated with clubbing
40
Q

adenocarcinoma of the lung in situ

A

bronchiolovar subtype of the adenocarcinoma

  • CXR:hazy infiltrated similar to pneumonia
  • apparent thickenin of alveolar walls.
41
Q

caitaiton , cigarret relate and hypercalcemia related lung cancer

A

squamos cell carcinoma

produces PTHrP

keratin pearls and intercelular bridges

42
Q

lung cancer with these three paraneoplasic syndromes :

ACTH

ADH

Lamber-Eaton

A

small cell(oat cell) carcinoma

  • central
  • amplified Myc
  • inoperable:treat with chemo
  • neuroendocrine neoplasm of kulchitsky cells->salt and paper aparience
43
Q

less responsive to chemoteraphy lung cancer higly anaplastic

A

large cell carcinoma

peropheral

44
Q

chromogranin A possitive lung cancer

A

Bronchial carcinoid tumor

not associated with cigarret

45
Q

intertitial pneumonia in transplanted patients

A

CMV pneumonia

  • diffuse patchy inflammation localized to interstitial areas at alveolar walls.
  • indolent course.
46
Q
A

Lung abscess

air-fluid levels often seen on CXR oftehn due to S.aureus or anaerobes.

47
Q

cuts S bound in mucus

A

N-acetylcysteine

48
Q

induces bronchodiltation by increasing cAMP

A

ß2 agonist

  • Alburetol
  • long acting:salmeterol, formeterol
49
Q

promotes bronchodilation by inhibitil PDE and decreasin hydrolysis os cAMP

A

Methylxantines

  • theophylline
  • blocks adenosine(adenosine cause bronchoconstriction)
50
Q

preven bronchoconstriction by inhibitin M3 muscarinic receptors

A

Muscarinic antagonis

  • short acting:ipatropium
  • long acting:Tiotropium
  • used in ARDS
51
Q
A

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