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FirstAID > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Anatomic dead space:

A

Conducting zone (nose, pharynx, trachea, bronchi, bronchioles, terminal bronchioles)

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2
Q

Conducting Zone:

A

Nose, pharynx, trachea, bronchi, bronchioles, terminal bronchioles

  • ->anatomic dead space (no gas exchange here)
  • ->warms, humidifies, filters air
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3
Q

Respiratory zone:

A

Respiratory bronchioles, alveolar ducts, alveoli

–>participates in gas exchange

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4
Q

What parts of the respiratory tree contain cartilage?

A

–>Trachea and Bronchi

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5
Q

What part of respiratory tree contains goblet cells?

A

goblet cells extend to the bronchi

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6
Q

Type I vs Type II pneumocytes:

  • cell type?
  • functions?
A
  • Type I: cover about 97% of alveolar surfaces
  • ->line alveoli
  • ->squamous cells
  • ->thin for optimal gas diffusion
  • Type II: only cover about 3% of alveolar surfaces
  • ->secrete surfactant (dipalmitoyl phosphatidylcholine)
  • ->cuboidal cells
  • ->precursors to both type I and other type II pneumocytes
  • ->proliferate during lung damage
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7
Q

Dipalmitoyl phosphatidylcholine

A

= pulmonary surfactant

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8
Q

Clara cells

A

nonciliated, columnar secretory cells

  • ->secrete component of surfactant
  • ->degrade toxins
  • ->act as reserve cells
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9
Q

Lecithin:Sphingomyelin ratio:

-significance? what’s a significant ratio?

A

L:C ratio > 2.0 in amniotic fluid –> indicates fetal lung maturity

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10
Q

What forms the Diffusion/Gas-exchange barrier between the capillary lumen and alveolar space?

A
  • Endothelial cells (tight junction)
  • Type I epithelial cells
  • Basement membrane
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11
Q

How far down respiratory tree are there ciliated cells (pseduostratified ciliated columnar cells)?

A

–>ciliated cells extend to the respiratory bronchioles

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12
Q

Which lung is more common site for an inhaled foreign body? why?

A

–>Right lung; b/c right main bronchus is wider and more vertical than left

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13
Q

Which lung has 3 lobes? 2 lobes? lingula?

A

right lung –> 3 lobes

left lung –> 2 lobes + lingula (homologue of right middle lobe); left lung needs space for the heart!

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14
Q

Which nerve/roots innervate diaphragm?

A

Phrenic: C3, C4, C5 keep the diaphragm alive!

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15
Q

Pain from diaphragm may be referred to where?

A

shoulder

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16
Q

Structures that perforate the diaphragm (and the levels at which they do so):

A

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

  • T8: IVC
  • T10: Esophagus + vagus
  • T12: Aorta + thoracic duct + azygous vein

***T12: Red, White, and Blue –> Aorta (red), Thoracic duct (white), Azygous vein (blue)

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17
Q

Which part of breathing is passive: inspiration or expiration?

A
  • ->expiration=passive

* inspiration uses the diaphragm!

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18
Q

3 functions of surfactant:

A
  • decrease alveolar surface tension
  • increase compliance
  • decrease work of inspiration
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19
Q

5 lung products:

A

1) Surfactant
2) Prostaglandins (relax bronchi)
3) Histamine (increases bronchoconstriction)
4) ACE (ang I–>ang II; and inactivates bradykinin)
5) Kallikrein (activates bradykinin)

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20
Q

Equation for Collapsing Pressure = P =

A

P= (2 X surface tension) / radius

***smaller radius–> increased tendency to collapse on expiration (law of Laplace)

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21
Q

Kallikrein:

A

Product of the lungs

–>activates bradykinin (vs ACE, also a product of the lung, which inactivates bradykinin!)

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22
Q

Prostaglandins vs Histamine:

A
  • ->both are products of the lung
  • Prostaglandins –> relax bronchi
  • Histamine –> stimulates bronchoconstriction
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23
Q

Are alveoli with smaller or larger radii more likely to collapse during expiration, without surfactant?

A

–>smaller radius–> more likely to collapse without surfactant

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24
Q

Vital Capacity =

A

VC = TLC - RV = IRV + TV + ERV

–>it’s maximal inspiration and expiration

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25
Q

Inspiratory Capacity =

A

IC = IRV + TV

–>maximum amount that can be inspired

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26
Q

Functional Residual Capacity =

A

FRC = ERV + RV

–> amount of air in lungs after a normal, tidal volume, expiration

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27
Q

Total Lung Capacity =

A

TLC = IRV + TV + ERV + RV

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28
Q

Calculation of Physiologic Dead Space = VD= ?

A

VD = [VT X (PaCO2 - PeCO2)] / PaCO2

“Taco Paco Peco Paco”

  • VD = physiologic dead space = anatomic dead space (conducting zone) + functional dead space in alveoli; it’s the volume of inspired air that doesn’t participate in gas exchange
  • VT = Tidal Volume
  • PaCO2 = arterial PCO2
  • PeCO2 = expired air PCO2
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29
Q

Which part of a healthy lung is the largest contributor to functional dead space?

A

–>Apex of healthy lung

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30
Q

Natural tendency of lungs and chest wall:

A

Lungs want to collapse inward

Chest wall wants to spring outward

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31
Q

Lung and Chest wall at FRC:

A 
At FRC (Functional Residual Capacity--> after a normal expiration): inward pull of lung is balanced with outward pull of chest wall; system pressure is atmospheric 
-->have negative intrapleural pressure at FRC; both airway and alveolar pressure = 0
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32
Q

What is compliance? How does it relate to FRC? What conditions are associated with decreased compliance?

A

Compliance = Change in lung volume for a given change in pressure

*decreased compliance –> decreased FRC

  • Decreased compliance in:
  • pulmonary fibrosis
  • insufficient surfactant
  • pulmonary edema
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33
Q

Adult hemoglobin, Fetal hemoglobin composition?

A

Adult Hb: 2alpha, 2beta subunits

Fetal Hb: 2alpha, 2gamma subunits

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34
Q

R and T forms of Adult Hb:

A
  • T form = Taut form = “Tissue form” –> has low affinity for O2; so increased O2 unloading into tissues… Right shift of Oxygen-Hb dissociation curve in T form (Increased Oxygen unloading)
  • R form = Relaxed form –> high affinity for O2
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35
Q

What conditions favor the T (taut) form of Hb?

A
  • ->anything that shifts Oxygen-Hb curve to right (increased O2 unloading):
  • increased temperature
  • increased 2,3-BPG
  • increased H+ (decreased pH)
  • increased Cl-
  • increased CO2
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36
Q

How does Fetal Hb differ from adult?

A

–>Fetal Hb has decreased affinity for 2,3-BPG than adult Hb, so has higher affinity for O2 (less O2 unloading)

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37
Q

Methemoglobin:

A

= Oxidized form of Hb (Ferric, Fe3+; normally iron in Hb is in a reduced state –> ferrous, Fe2+ (Ferrou2))

*Methemoglobin has increased affinity for Cyanide; decreased affinity for O2

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38
Q

Ferric vs Ferrous state of iron in Hb:

A

Ferric = Fe3+ –> oxidized form = Methemoglobin

Ferrous = Fe2+ –> reduced form of iron; normal form of Hb; binds O2 well

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39
Q

Treatment for Methemoglobinemia:

A
  • Methylene Blue

- Vitamin C

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40
Q

Treatment for Cyanide Poisioning:

A

-Nitrites (oxidize Hb to Methemoglobin–> has increased affinity for CN-, so Hb binds cyanide –> allows cytochrome oxidase to fxn)

Then, give:

-Thiosulfate –> binds cyanide forming thiocyanate, which is renally excreted

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41
Q

Carboxyhemoglobin:

A
  • ->Hb bound to CO instead of O2
  • decreases oxygen-binding capacity and decreases oxygen unloading to tissues (Left shift in Oxygen-Hb dissociation curve)

***CO has 200X greater affinity than O2 for Hb!!!

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42
Q

Factors that cause a Right shift in the Oxygen-Hb dissociation curve:

A

“C-BEAT”

  • increased CO2
  • increased 2,3-BPG
  • Exercise
  • increased Acidity (increased H+, decreased pH)
  • increased Temperature
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43
Q

How does the presence of CO affect Hb saturation?

A

Have increased Hb saturation at any given PO2 in the presence of CO, b/c of positive cooperativity

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44
Q

Normal resistance and compliance in pulmonary circulation:

A

Low resistance, High compliance (normally)

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45
Q

Effect of decreased PAO2

A

Hypoxic VasoCONSTRICTION (shifts blood away from poorly ventilated parts of lung to well-ventilated parts of lung)

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46
Q

Perfusion-limited vs Diffusion-limited Pulmonary circulation:

A
  • Diffusion-limited: based on how much blood is flowing through (increased blood flow –> increased diffusion)
  • Diffusion-limited: based on gas exchange (ie in emphysema, fibrosis–> decreased gas exchange)
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47
Q

Equation for Diffusion = Vgas = ?

A

Vgas = (A/T) X Dk(P1-P2)

A=Area
T=Thickness
Dk(P1-P2) = difference in partial pressures

  • **decreased A in emphysema
  • **increased T in fibrosis
  • ->SO: both of these conditions lead to decreased diffusion
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48
Q

Normal pulmonary artery pressure?

A

10-14 mmHg

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49
Q

Pulmonary hypertension: pulmonary artery pressure?

A

> or = 25 mmHg

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50
Q

Results of pulmonary HTN (how does it affect pulmonary arteries?):

A
  • Atherosclerosis
  • Medial hypertrophy
  • Intimal fibrosis
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51
Q

BMPR2 (Bone Morphogenic Protein Receptor type 2)

A

genes that is mutated in primary pulmonary hypertension (it is inactivated)

BMPR2 gene normally inhibits vascular smooth muscle proliferation; but, in primary pulmonary HTN it is inactivated… so get excess vascular SM proliferation
–>poor prognosis

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52
Q

Cause of primary pulmonary HTN?

A

inactivating mutation of BMPR2 gene (get excess vascular smooth muscle proliferation)

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53
Q

Causes of secondary pulmonary HTN?

A
  • COPD (destruction of lung parenchyma)
  • Mitral stenosis (increased resistance in left heart –> get increased pressure which backs up into the lungs)
  • Recurrent thromboemboli (results in decreased cross-sectional area of pulmonary vascular bed)
  • Autoimmune disease (inflammation–> intimal fibrosis –> medial hypertrophy)
  • Left to Right shunt in the heart
  • sleep apnea or living at high altitudes (hypoxic vasoconstriction)
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54
Q

Course of progression of pulmonary HTN:

A

severe respiratory distress –> cyanosis and RVH –> decompensated cor pulmonale, resulting in death

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55
Q

Pulmonary Vascular Resistance equation: PVR = ?

A

PVR = (Ppulm artery - PL atrium) / CO

  • Ppulm artery = pressure in the pulmonary artery
  • PL atrium = pulmonary wedge pressure
  • CO = cardiac output
  • **R = delta P/Q
  • -> Resistance = change in pressure / Flow

***Resistance is proportional to viscosity and vessel length; inversely proportion to radius^4

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56
Q

Oxygen content of blood = ?

A

O2 content = (O2 binding capacity to Hb X %saturation of Hb) + dissolved O2

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57
Q

When have decreased Hb (ie anemia), how does it affect:

  • O2 content of arterial blood?
  • O2 saturation?
  • arterial PO2?
A
  • decreased O2 content of arterial blood

- NORMAL O2 saturation and arterial PO2

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58
Q

How does exercise affect PO2?

A

Exercise decreases venous PO2 (makes sense –> have increased delivery of Oxygen to tissues, so less O2 in VENOUS blood going back to the lungs)

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59
Q

How does chronic lung disease affect PO2?

A

Have decreased PO2 in arterial blood (makes sense, b/c have decreased diffusion of Oxygen into blood in the lungs, so less oxygen in the arteries…)

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60
Q

Oxygen delivery to tissues = ?

A

O2 delivery to tissues = CO X O2 content of blood

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61
Q

Alveolar gas equation (approximate): PAO2 =? (know!!! :))

A

PAO2 = 150 - PaCO2/0.8

*note: this is an approximation (if pt has increased O2 - like an oxygen mask - then >150; if pt has decreased O2 - like high altitude - then <150)

  • PAO2 = alveolar PO2
  • PaCO2 = arteriolar PCO2
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62
Q

A-a gradient (Alveolar-arterialor gradient) =

A

A-a gradient = PAO2 - PaO2

*should = 10-15 mmHg

–>Increased A-a gradient is BAD! Get increased A-a gradient in hypoxemia (have oxygen in alveoli, but not making it into arterioles) –> may be d/t a shunt in the heart (so, oxygenated blood sent back to lungs), V/Q mismatch, fibrosis (impairs diffusion), etc…

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63
Q

Hypoxemia vs Hypoxia vs Ischemia:

A
  • Hypoxemia = decreased PaO2 (arterial O2)
  • Hypoxia = decreased O2 delivery to tissues
  • Ischemia = Loss of blood flow
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64
Q

4 ways to get Hypoxemia (Low PaO2):

A

1) alveolar hypoventilation (have a normal A-a gradient though, b/c diffusion, etc, is not the problem)
2) V/Q (ventilation/perfusion mismatch)
3) Diffusion impairment
4) Right –> Left shunting in the heart

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65
Q

V/Q (ventilation/perfusion):

  • ideal ratio = ?
  • ratio at apex of the lung = ?
  • ratio at base of the lung = ?
A
  • ideally, V/Q = 1 (matched ventilation and perfusion)
  • Apex of the lung: V > Q –> V/Q = 3 (have wasted ventilation; have more air in apex than blood –> why TB looooves it :))
  • Base of lung: V < Q –> V/Q = 0.6 (wasted perfusion; have more blood than air; BOTH V and Q are increased at the base; BUT, Q increases more than V, so get lower V/Q ratio)
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66
Q

V/Q ratio during exercise?

A

V/Q ratio approaches 1 during exercise/increased CO (b/c have vasodilation of apical capillaries, so higher Q/perfusion)

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67
Q

V/Q ratio in airway obstruction/shunt?

A

V/Q approaches 0

b/c can’t ventilate… even if give 100% O2, won’t help

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68
Q

V/Q ratio in blood flow obstruction/physiologic dead space?

A

V/Q approaches infinity
(b/c very little perfusion, low Q; is helped if given 100% O2, if there is some part of the lung that can undergo diffusion/is perfused)

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69
Q

Form in which most blood CO2 is transported?

A

CO2 is carried as bicarbonate in the plasma

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70
Q

3 forms that CO2 is transported from tissues to lungs:

A

1) Bicarbonate (90% is transported this way! carried in the plasma)
2) CO2 bound to hemoglobin at N-terminus; CO2 binding to Hb favors the Taut formation of Hb (favoring O2 unloading) (about 5%)
3) Dissolved CO2 (about 5%)

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71
Q

Pulmonary/gas exchange responses to high altitude:

A

1) Increase in ventilation (decreased PO2 and PCO2)
2) Increased EPO (not if pt has kidney failure!) –> get increased Hct and Hb (d/t chronic hypoxia)
3) increased 2,3-BPG –> so, increased O2 unloading to tissues
4) Increased mitochondria within cells
5) increased renal excretion of bicarbonate, to compensate for respiratory alkalosis (can help this out by giving Acetazolamide!)
6) Chronic hypoxic pulmonary vasoconstriction results in RVH (and eventually cor pulmonale)

72
Q

Pulmonary/Gas exchange responses to Exercise:

A

1) increased CO2 production
2) increased O2 consumption
3) increased ventilation rate (b/c increased O2 demand)
4) V/Q ratio approaches 1 (becomes more uniform from apex to base)
5) increased pulmonary blood flow (to increase CO)
6) decreased pH during strenuous exercise (result of lactic acidosis)
7) Increased CO2 content; but, no change in PaO2 and PaCO2

73
Q

Types of emboli:

A

“FAT BAT”

  • Fat
  • Air (like from Bends/scuba diving)
  • Thrombus
  • Bacteria (like from bacterial endocarditis)
  • Amniotic fluid (may lead to DIC post-partum)
  • Tumor
74
Q

Pt with recent long-bone or pelvic fracture + Triad: acute-onset neuro abnormalities + hypoxemia + petechial rash:

A

Fat embolism syndrome

75
Q

Lines of Zahn:

A

–>characteristic of thrombi, especially in the heart or aorta; have alternating layers of RBCs, platelets, and fibrin, so have layers of reds and pinks.

76
Q

Stasis + Hypercoagulability + Endothelial damage –> predispose to what condition?

A

DVT

*this is “Virchow’s triad”

77
Q

Prevention and treatment for DVT?

A

–>Heparin!

78
Q

Homan’s sign:

A

when dorsiflex foot, have tender calf muscle = sign of DVT

79
Q

FVC = Forced Vital Capacity:

A

the maximum volume of air that can be forcefully exhaled (Vital capacity when force as much air out as can)

80
Q

FEV1 =

A

volume of air exhaled in the first second of forced expiration

81
Q

FEV1/FVC ratio:

A

–>represents volume of air exhaled in first second of expiration, over the total amount expired. Normally it’s about 80%

  • In obstructive lung diseases: ratio is decreased
  • In Restrictive lung diseases: ratio is increased
82
Q

Obstructive Lung Diseases (COPD):
-Includes which diseases?
-What are the hallmarks (PFTs: FEV1,
FVC, FEV1/FVC, V/Q, etc…)

A
  • Obstructive lung diseases:
  • chronic bronchitis
  • emphysema
  • asthma
  • bronchectasis
  • Hallmarks:
  • increased RV (so increased volume of air in lungs, even after maximal expiration)
  • decreased FVC (maximal amount of air that can be exhaled is decreased)
  • very decreased FEV1 (»>FVC decrease) –> volume of air exhaled in 1st second is decreased
  • V/Q mismatch

***Overall: decreased FEV1/FVC ratio (both are decreased, but FEV1 is decreased more than FVC)

83
Q

Chronic Bronchitis:

  • dx/presentation?
  • pathology?
A
  • productive cough for > 3 consecutive months over at least 2 years
  • wheezing, crackles, cyanosis (“Blue Bloater”), dyspnea
  • hypertrophy of mucus-secreting glands in bronchioles (it’s a disease of small airways); such that more than half of the bronchial wall is composed of mucus-secreting glands
84
Q

Reid Index =

A

=gland depth / total thickness of bronchial wall

In COPD/Chronic Bronchitis: Reid index > 50% (meaning, more than half of the bronchiole wall is comprised of mucus secreting glands)

85
Q

Emphysema:

  • pathology?
  • presentation?
A

= “pink puffer”
–>Destruction of alveolar walls, so get enlargement of air spaces (enlarged alveoli with thin septa), decreased recoiling and decreased compliance (have increased elastase activity, and thus loss of elastic fibers, which causes the increased compliance

*pts exhale through pursed lips (b/c it increases airway pressure and prevents airway collapse during respiration)

86
Q

Methacholine challenge:

A

Test for making asthma dx:
have pt breath in methacholine, which causes bronchoconstriction. In asthmatics, have pre-existing airway hyper-reactivity, so react with bronchonconstriction at lower doses of the drug.

87
Q

Inspiration:Expiration ratio in Asthma:

A

–>decreased I:E ratio (so, shorter inspirations, longer expirations)

88
Q

Asthma:

  • pathology
  • presentation
A
  • Asthma = inflammation + bronchoconstriction
  • have smooth muscle hypertrophy and mucus plugging (“Curschmann’s spirals”)
  • cough, wheezing, tachypnea, dyspnea, hypoxemia
  • decreased I:E ratio, pulsus paradoxus (drop in systolic pressure > 10 mmHg), mucus plugging.
89
Q

Bronchiectasis:

  • what is it?
  • presentation?
  • associated with what conditions?
  • complications?
A
  • chronic necrotizing infection of bronchi, so have permanently dilated airways, purulent sputum, recurrent infections (ie pseudomonas), hemoptysis
  • Associated with smoking (poor ciliary motility), Karatagener’s (poor ciliary motility), CF, bronchial obstruction
  • May lead to Aspergillosis!!!
90
Q

Panacinar vs Centri-acinar Emphysema:

A
  • Panacinar –> d/t alpha-1-antitrypsin deficiency (so get increased elastase activity –> decreased elastin –> destroys entire acini)
  • get emphysem + liver cirrhosis at early age (20-30s)

*Centri-acinar: d/t smoking; only central part of acini destroyed

***“acini” = clusters of alveoli

91
Q

Restrictive Lung Diseases:

  • hallmarks? (PFTs)
  • 2 main categories of Restrictive lung diseases:
A
  • have DECREASED lung volumes, so decreased FVC and TLC
  • PFTs: increased FEV1/FVC ratio (>80%)
  • Types:
    1) poor breathing mechanics (has to do with extrapulmonary factors):
  • poor muscular effort (ie polio, myasthenia gravis, guillain-barre…)
  • poor structural apparatus (like obesity, scoliosis)
    2) interstitial lung disease (has to do with pulmonary factors, like decreased diffusing capacity):
  • ARDS
  • Neonatal RDS = hyaline membrane disease
  • pneumoconioses (coal miners, silicosis, asbestosis)
  • sarcoidosis
  • idiopathic pulmonary fibrosis
  • Goodpasture’s
  • Wegener’s
  • granulomas (histiocytosis X)
  • drug toxicities that cause pulmonary fibrosis (bleomycin, amiodarone, busulfan)
92
Q

3 drugs that can cause pulmonary fibrosis, and thus interstitial lung disease:

A
  • bleomycin (anti-tumor antibiotic; induces free radical formation, used to treat testicular cancer)
  • amiodarone (class III antiarrhythmic)
  • busulfan (antitumor drug, alkylating agent; used to treat CML and to ablate pts BM before BM transplant)
93
Q

PFTs of Obstructive vs Restrictive Lung Diseases:

A

Obstructive:

  • increased lung volumes
  • increased RV
  • decreased FEV1 and FVC (but FEV1 more decreased than FVC)
  • ->decreased FEV1:FVC ratio
  • V/Q mismatch
  • Restrictive:
  • decreased lung volumes
  • decreased FVC and TLC
  • ->increased FEV1:FVC ratio (>80%)
94
Q

Which part of lungs is affected in pneumoconioses: coal miner’s? asbestosis? silicosis?
*Which of the pneumoconioses are associated with increased risk of cancer? (and which cancers?)

A
  • Coal miner’s and silicosis –> affect upper lobes of lung; NO increased risk of lung cancer
  • Asbestosis –> affects lower lobes of lungs; associated with increased risk of mesothelioma and bronchogenic carcinoma
95
Q

2 lung cancers associated with asbestos exposure?

A
  • bronchogenic carcinoma

- mesothelioma

96
Q

“eggshell” calcification of hilar lymph nodes; disrupted phagolysosomes and impaired macrophages (causing the damage): Which pneumoconiosis?

A

Silicosis

  • ->macrophages cause the damage! macrophages respond to silica and release fibrogenic factors, leading to fibrosis
  • ->may have increased susceptibility to TB d/t impaired phagolysosomes and impaired macrophages!
97
Q

3 exposures associated with silicosis:

A
  • foundries (factories that produce metal casting)
  • sandblasting
  • mines (note coal miner’s lung is associated with coal mines)
98
Q

Exposure to what substance may increase risk of TB?

A

–>Silica; in silicosis, silica disrupts phagolysosomes and macrophages, so may increase susceptibility to TB

99
Q

Coal Miner’s lung may result in what 2 complications?

A
  • cor pulmonale

- Caplan’s sydnrome (rheumatoid arthritis involvement)

100
Q

Golden-brown fusiform rods that look like dumbbells within macrophages:

A

Asbestosis (macrophages cause the damage!)

101
Q

“ivory white” calcified pleural plaques:

A

–>Asbestosis

102
Q

What gestational month is surfactant produced?

A

–>surfactant is most abundantly produced >35 weeks gestation

103
Q

Lecithin:Sphinogmyelin ratio in neonatal RDS?

A

L:S < 1.5 in neonatal RDS (Hyaline Membrane Disease)

L:S > 2.0 indicates lung maturity…

104
Q

Causes of Acute Respiratory Distress Syndrome (adults)?

A

–>anything that causes severe damage to lungs/injury to endothelial cells in lungs

  • trauma, sepsis, shock
  • gastric aspiration
  • uremia
  • Acute Pancreatitis! (***)
  • Amniotic fluid embolism
105
Q

Pathology of ARDS:

A

Damage to alveoli/endothelial cells–> increased alveolar capillary permeability –> protein-rich leakage into alveoli –> get formation of intra-alveolar hyaline membrane

***Immune-system-mediated damage: the initial damage to the alveoli is d/t release of neutrophilic substances that are toxic to the alveolar wall, coagulation cascade, and oxygen-derived free radicals

*SO: inflammatory cells cause the alveolar damage!

106
Q

Central vs Obstructive Sleep Apnea:

A
  • Central –> no respiratory effort (see in preemie infants)
  • Obstructive –> respiratory effort against obstruction of airways (like soft palate, uvula, enlarged tonsils block airway)

***Note: Hypoxia –> Increased EPO –> Increased Erythrocytosis

***Treat Obstructive with: weight loss, CPAP, surgery

107
Q

Absent/Decreased breath sounds over area in lungs + decreased resonance + decreased fremitus + tracheal deviation toward side of lesion:

A 
Bronchial obstruction
(air can't get into lesioned part of lung; have collapse in that area, so trachea goes towards the side of lesion, b/c more space there (it's not inflate))
108
Q

Decreased breath sounds + Dullness + decreased fremitus:

A

Pleural effusion (fluid b/w lung and chest wall)

109
Q

Dullness + Increased fremitus:

A

Lobar Pneumonia

110
Q

decreased breath sounds + Hyper-resonant + No fremitus + Tracheal deviation away from side of lesion:

A

Tension pneumothorax
(trachea deviates AWAY b/c have increased air in pleural space on side of pneumothorax; so everything gets pushed over to the other side)

111
Q

Decreased breath sounds + Hyper-resonant + decreased fremitus + Trachea deviates toward side of lesion:

A

–>Spontaneous pneumothorax (trachea deviates toward side of lesion, b/c lung is collapsed, so more space on that side…)

112
Q

Leading cause of Cancer death?

A

Lung Cancer

113
Q

Primary tumors that commonly metastasize to lungs:

A

Breast, Colon, Prostate, Bladder

114
Q

Sites that lung cancer may metastasize to:

A

Adrenals, brain, bone, liver

115
Q

Complications of lung cancer:

A

“SPHERE of complications”

  • Superior vena cava syndrome (SVC gets compressed)
  • Pancoast tumor
  • Horner’s syndrome
  • Endocrine (paraneoplastic)
  • Recurrent laryngeal symptoms (ie hoarseness)
  • Effusions (pleural, pericardial)
116
Q

Lung cancer that may cause ectopic production of ACTH or ADH?

A

–>Small cell carcinoma

117
Q

Lung cancer that may lead to Lambert-Eaton syndrome (by producing autoantibodies against Calcium channels)?

A

–>Small Cell carcinoma

118
Q

Small Cell Carcinoma:

  • where in lungs is it located?
  • what conditions is it associated with/can it lead to?
  • Prognosis?
  • histology of cells?
A
  • Central location (“S lung cancers are located Sentrally”)
  • associated with ectopic production of ACTH, ADH, and autoantibodie to calcium channels (causing Lambert-Eaton syndrome)
  • Poor prognosis; inoperable, very aggressive; responsive to chemo though
  • Histology: small dark blue cells (“Kulchitsky cells”); have high nucleus:cytoplasm ratio –> very little cytoplasm
119
Q

Lung cancers that are NOT associated with smoking?

A

Bronchial and Bronchioalveolar Adenocarcinomas

120
Q

Most common lung cancer in NON-smokers and Females?

A

Bronchial Adenocarcinoma

–>presents in places where had prior pulmonary inflammation or injury

121
Q

Which types of lung cancer are Centrally located?

A

“S cancers are Sentrally located”

  • Small Cell (Oat Cell) Carcinoma
  • Squamous Cell Carcinoma
122
Q

Which types of lung cancer are Peripherally located?

A
  • Adenocarcinomas (Bronchial and Bronchoalveolar)

- Large Cell carcinoma

123
Q

Keratin pearls on histology?

A
  • ->Squamous cell carcinoma

* **note: ANY squamous cell carcinoma (ie skin, lungs, etc…) has keratin pearls on histology

124
Q

Lung cancer with PTHrP (PTH-related protein), so get PTH effects:

A

Squamous Cell Carcinoma

125
Q

C’s and S’s of Squamous Cell Carcinoma of the lung:

A
  • Central (near hilum of lung)
  • Smoking
  • Cavitations
126
Q

Histology: pleomorphic giant cells with leukocyte fragments in cytoplasm: Which lung cancer?

A

Large cell carcinoma (Giant = Large cells…)

–>very bad prognosis; really undifferentiate, anaplastic tumor; can be removed surgically though

127
Q

Lung cancer that may cause:

  • Bronchospasm and wheezing
  • Flushing
  • Diarrhea
  • Right-sided heart lesions/murmurs (ie tricuspid insufficiency, pulmonary stenosis, right-heart failure)
A

Carcinoid tumor

  • ->secretes serotonin, causing carcinoid syndrome
  • ->get R-heart symptoms d/t fibrous deposits in R heart valves

***Most common sites of Carcinoid tumor = GIT and lungs (though, it is the most common tumor of the appendix)

128
Q

Lung Cancer with Psammoma bodies on histology?

A

Mesothelioma

–>associated with asbestos exposure!

129
Q

Pancoast tumor:

A
  • ->occurs in apex of lung

- ->may affect cervical plexus –> Horner’s syndrome (ptosis+ miosis + anhidrosis; usually unilateral)

130
Q

Superior Vena Cava syndrome:

A

Obstruction of SVC, d/t neoplasms usually or thromboses.

  • ->get facial swelling (b/c obstruction of blood drainage from head)
  • ->swelling of neck = jugular venous distention (again, can’t drain blood from head)
  • ->edema of upper extremities (again, can’t drain blood from upper parts of body)

***may increase ICP, if severe –> headaches, dizziness, and increased risk of aneurysm/rupture of arteries in brain.

131
Q

Most common causes of Lobar pneumonia (pneumonia involving both lungs; have intra-alveolar exudate):

A 
#1 cause = Strep pneumonia
-->also, Klebsiella
132
Q

Causes of Bronchopneumonia (acute inflammatory infiltrates; patchy distribution, involving 1 or more lobe):

A
  • Staph aurues
  • H. inlfuenza
  • Klebsiella
  • GAS
133
Q

Main causes of Interstitial/Atypical/Walking pneumonia (diffuse patchy inflammation in inerstitial areas of alveolar walls; involves 1 or more lobes; x-ray looks worse than symptoms):

A
  • Mycoplasma
  • Legionella
  • Chlamydia
  • Viruses (RSV, Adenovirus)
134
Q

Causes of Lung Abscesses (both microbes and not):

A
  • Microbes:
  • S. aureus
  • Anaerobes (bacteriodes, fusobacterium, peptostreptococcus)
  • Other causes:
  • aspiration of oropharyngeal contents (like in alcoholics or epileptics)
  • broncial obstruction (ie cancer)
135
Q

Transudate vs Exudate:

A
  • Transudate –> low protein content

- Exudate –> high protein content

136
Q

When might one get transudate (low protein) pleural effusion?

A
  • CHF
  • Nephrotic syndrome
  • Hepatic cirrhosis
137
Q

When might one get exudate (high protein) pleural effusion?

A
  • lobar pneumonia
  • malignancy
  • collagen vascular disease
  • trauma
138
Q

When might one get lymphatic pleural effusion (looks milky white!)

A

–>rupture of thoracic duct…

139
Q

What type of pneumothorax may be seen in tall, thin, young males?

A

–>spontaneous pneumothorax (trachea deviates toward side of affected lung)

140
Q

1st gen vs 2nd gen anti-histamines:

A

–>both are reversible H1 receptor blockers

  • 1st gen:
  • more side effects, b/c also blocks other pathways (anti-muscarinic, anti-alpha-adrenergic, anti-serotonergic)–> so get: blurry vision, dry mouth, urinary retention, appetite stimulation (DON’t give to elderly pts, b/c of anti-muscarinic effects!)
  • 1st gen can cross BBB –> sedation + cognitive dysfxn
  • 2nd gen:
  • fewer side effects, b/c don’t cross BBB (so, better for elderly pts)–> no sedation; more specific to H1 receptor; no anti-muscarinic, anti-serotonergic, anti-alpha-adrenergic properties/effects
141
Q

Which type of anti-histamine is preferred for elderly pts?

A

2nd generation anti-histamines

142
Q

Which type of anti-histamine can be given as a sleep aid?

A

1st generation (2nd generation doesn’t cross BBB; is only used for allergy trtmnt)

143
Q

List the 1st generation anti-histamines:

A
  • Diphenyhdramine (Benadryl)
  • Dimenhydrinate
  • Chlorpheniramine
144
Q

List the 2nd generation anti-histamines:

A
  • Loratidine
  • Fexofenadine
  • Desloratidine
  • Cetirizine
145
Q

Bosentan

A

Drug used to treat Pulmonary HTN

–>competitive blocker of endothelin-1 receptors; so decreases pulmonary vascular resistance

146
Q

Isoproterenol

A

non-specific B-agonist

  • ->used to treat asthma
  • ->relaxes bronchial smooth muscle (via Beta-2)
  • ->side effect = Tachycardia (via Beta-1)
147
Q

Albuterol:

A
  • Beta-2 agonist
  • ->treatment of acute asthma exacerbation
  • ->bronchodilation (relaxes bronchial smooth muscle) b/c acts on Beta-2 receptors (at really high doses, may get some Beta-1 effects…)
148
Q

Salmeterol

A

Beta-2 agonist

  • ->used for asthma prophylaxis
  • adverse effects = tremor and arrhythmia (d/t some Beta-1 effects too…)
149
Q

Theophylline:

A
  • causes bronchodilation by inhibiting phosphodiesterase –> so decreases cAMP hydrolysis (so, increased cAMP–> increased bronchodilation!)
  • used as a last resort in asthma trtmnt, b/c has a narrow TI, may lead to cardiotoxicity and neurotoxicity
150
Q

Ipratropium:

A
  • anti-muscarinic drug; can be used to treat asthma and COPD
  • ->prevents bronchoconstriction

“I pray (Ipra) I can breath soon!”

151
Q

Cromolyn:

A

–>drug used for asthma prophylaxis (Not for acute attacks, because take a while to kick-in)

  • mechanism: prevents release of mediators from mast cells
  • toxicity is rare, so can find OTC
152
Q

1st line therapy for Chronic Asthma?

A

–>Corticosteroids (Beclomethason, Prednisone, Fluticasone)

*Mechanism: inhibit synthesis of cytokines; inactivate the transcription fact (NF-KB)that induces production of TNF-alpha and other inflammatory agents

***So, basically: decrease TNF-alpha production!

153
Q

Zileuton:

  • use?
  • mechanism?
A

Drug used to treat asthma
–>anti-leukotriene: blocks 5-lipoxygenase pathway; so blocks conversion of arachidonic acid to leukotrienes (so, decreased inflammation)

154
Q

Zafirlukast:

  • use?
  • mechanism?
A

Used to treat asthma, especially aspirin-induced asthma

–>anti-leukotriene drug: blocks leukotriene receptor, so decreased inflammation

155
Q

Montelukast:

  • use?
  • mechanism?
A

Like Zafirlukast; drug used to treat asthma, especially aspirin-induced asthma
–>anti-leukotriene: blocks leukotriene receptors; so, decreased inflammation

156
Q

Drugs used to treat aspirin-induced asthma?

A

–>antileukotrienes: Zafirlukast and Montelukast

157
Q

Guaifenesin:

A

Exectorant
–>removes excess sputum (but no effect on cough)

*found in Robitussin!

158
Q

Guaifenesisn + Dextromethorphan:

A

–>found together in Robitussin DM –> expectorant + cough suppressant!

159
Q

N-acetylcysteine:

A
  • ->antidote for acetaminophen overdose (b/c regenerates glutathione)!
  • AND*
  • ->can loosen mucus plugs in CF pts (an expectorant)
160
Q

Dextromethophan:

A
  • ->opioid analgesic; synthetic codeine analog (so,mild abuse potential)
  • ->used as a cough suppressant; found in Robittusin (DM)
  • ->mechanism = antagonizes NMDA glutamate receptors
  • ->if OD: give Naloxone
161
Q

Methacholine:

A
  • -> Muscarinic receptor agonist

- -> used for asthma challenge test (causes bronchoconstriction; at low doses in asthmatic pts)

162
Q

Pseudoephedrine and Phenylephrine:

  • mechanism?
  • uses?
  • toxicity?
A

*alpha-agonists
*used for nasal congestions, etc. also, opens eustachian tubes (think about me, sudafed, ears after airplane!)
*toxicity:
-HTN (b/c alpha agonist–> alpha 1 => increased BP)
-Pseudoephedrine may cause CNS stimulation/anxiety
-

163
Q

Diphenhydramine

A

1st generation anti-histamine

164
Q

Loratidine

A

2nd generation anti-histamine

165
Q

Chlorpheniramine

A

1st generation anti-histamine

166
Q

Fexofenadine

A

2nd generation anti-histamine

167
Q

Cetirizine

A

2nd generation anti-histamine

168
Q

Dimenhydrinate:

A

1st generation anti-histamine

169
Q

Methacholine:

A
  • -> Muscarinic receptor agonist

- -> used for asthma challenge test (causes bronchoconstriction; at low doses in asthmatic pts)

170
Q

Pseudoephedrine and Phenylephrine:

  • mechanism?
  • uses?
  • toxicity?
A

*alpha-agonists
*used for nasal congestions, etc. also, opens eustachian tubes (think about me, sudafed, ears after airplane!)
*toxicity:
-HTN (b/c alpha agonist–> alpha 1 => increased BP)
-Pseudoephedrine may cause CNS stimulation/anxiety
-

171
Q

Diphenhydramine

A

1st generation anti-histamine

172
Q

Loratidine

A

2nd generation anti-histamine

173
Q

Chlorpheniramine

A

1st generation anti-histamine

174
Q

Fexofenadine

A

2nd generation anti-histamine

175
Q

Cetirizine

A

2nd generation anti-histamine

176
Q

Dimenhydrinate:

A

1st generation anti-histamine

FirstAID (24 decks)

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