Bsom Pulmonary Markus 2010

Front 1

what is the function of the conchae in the lateral wall

Back 1

increase surface area and create turbulent airflow to maximize warming and filtering of entering air

Front 2

What type of epithelium is the respiratory epithelium

Back 2

pseudostratified columnar epithelium

Front 3

what is the mucociliary escalator

Back 3

moves mucus from nasal cavity towards the oropharynx and from the lower respiratory towards the pharynx

Front 4

what are the purpose of swell organs in the nasal mucosa

Back 4

large venous sinuses of the mucosa over the concha form erectile tissue that affects passage of air through the nasal cavity

Front 5

the hard palate is made of 2 types of epithelium, one type on the upper surface and one on the lower surface. Describe the different types

Back 5

upper surface- respiratory epithelium (pseudostratified columnar )

lower surface- stratified squamous

Front 6

what is the composition of the soft palate

Back 6

muscle, aponeurosis, and mucous membrane

Front 7

what are the 5 muscles of the soft palate

Back 7

1. musculus uvulae

2. palatoglossus

3. levator veli palatini

4. tensor veli palatini

Front 8

which 3 muscles act to lift the pharynx during swallowing

Back 8

1. stylopharyngeus

2. palatophrayngeus

3. salpingopharyngeus

Front 9

which nerve innervates the cricothyroid. What is the embyonic origins

Back 9

CN X- superior branch of the vagus

Muscles of mesoderm from arch 4 are pharyngeal constrictors, cricothyroid, levator veli palatinini

Arteries from mesoderm of Arch 4- Arch of the aorta, R. subclavian, sprouts of pulmonaries

Arch 4 Pouch endoderm--> superior parathyroids

Connective tissue from neural crest of Arch 4- thyroid cartilage

Front 10

which nerve innervates the intrinsic larynx. What are the embyonic origins

Back 10

Recurrent laryngeal nerve of the Vagus

Muscles of mesoderm from arch 4 are all the laryngeal constrictors, NOT THE cricothyroid,

Arteries from mesoderm of Arch 4- ductus arteriosus, definitive pulmonary arteries

Connective tissue from neural crest of Arch 4- cricoid cartilage

Front 11

which type of epithelium is on the following structures

nasopharynx

a. respiratory epithelium- cilicated pseudostratified

b. stratified squamous non-ketatinized

c. stratified squamous ketatinized

Back 11

a. respiratory epithelium- cilicated pseudostratified

Front 12

which type of epithelium is on the following structures

oropharynx

a. respiratory epithelium- cilicated pseudostratified

b. stratified squamous non-ketatinized

c. stratified squamous ketatinized

Back 12

b. stratified squamous non-ketatinized

Front 13

which type of epithelium is on the following structures

larynx

a. respiratory epithelium- cilicated pseudostratified

b. stratified squamous non-ketatinized

c. stratified squamous ketatinized

Back 13

b. stratified squamous non-ketatinized

Front 14

Name the action:

Must close the oropharyngeal isthmus

Palatoglossus and palatopharyngeus depress palate and move arches towards
midline

Palatoglossus also raises back of tongue

a. normal breathing
b. Breathing with food or liquid in oral cavity
c. Swallowing

Back 14

b. Breathing with food or liquid in oral cavity

Front 15

Name the action

Must close the pharyngeal isthmus and open the oropharyngeal isthmus

Tensor palatini makes soft palate firm

Levator palatini raises palate above the horizontal

Larynx elevated to push epiglottis against root of tongue, closing inlet

a. normal breathing
b. Breathing with food or liquid in oral cavity
c. Swallowing

Back 15

c. Swallowing

Front 16

t/f Trachea and bronchi have complete cartilaginous rings to prevent the trachea from collapsing during absence of air and for protection

Back 16

false- incomplete C shaped rings to prevent collapse and for protection

Front 17

Oblique fissure separates which lobes

Back 17

Oblique fissure separates superior and inferior lobes

Front 18

Horizontal fissure defines which lobe

Back 18

Horizontal fissure defines middle lobe of right lung

Front 19

List the components of the conducting zone of the respiratory tree

Back 19

1. nose

2. pharynx

3. trachea- cartilage

4. bronchi- cartilage

5. bronchioles

6. terminal bronchioles

Front 20

which components of the conducting zone of the respiratory tree have cartilage

Back 20

3. trachea- cartilage

4. bronchi- cartilage

Front 21

what is the function of the conducting zone of the respiratory tree

Back 21

brings air in and out, warms, humidifies, and filters the air

Front 22

t/f wall of the conducting zone contain skeletal muscle

Back 22

false- contain smooth muscle

Front 23

List the components of the respiratory zone of the respiratory tree

Back 23

1. respiratory bronchioles

2. alveolar ducts

3. alveoli

Front 24

what is the function of the respiratory zone of the respiratory tree

Back 24

respiration, gas exchange

Front 25

t/f Conducting bronchioles have cartilage and glands

Back 25

false- Conducting bronchioles (no cartilage or glands) —›

Front 26

name the portion of the respiratory tract

typical respiratory epithelium with lots of mixed glands

hyaline cartilage rings

a. trachea
b. bronchial tree
c. bronchioles
d. alveoli

Back 26

a. trachea

Front 27

name the portion of the lower respiratory tract

decrease in cartilage

increase in smooth muscle and elastic fibers

decreased cell height and number of glands

Back 27

b. bronchial tree

Front 28

name the portion of the lower respiratory tract

no cartilage or glands

a. trachea
b. bronchial tree
c. bronchioles
d. alveoli

Back 28

c. bronchioles
d. alveoli

Front 29

Name the portion of the bronchioles

pseudostratified columnar epithelium –› ciliated simple
columnar with goblet cells

a. conducting bronchioles
b. terminal bronchioles
c. respiratory bronchioles
d. alveolar ducts

Back 29

a. conducting bronchioles

Front 30

Name the portion of the bronchioles

ciliated cuboidal cells with Clara cells (secretory)

a. conducting bronchioles
b. terminal bronchioles
c. respiratory bronchioles
d. alveolar ducts

Back 30

b. terminal bronchioles

Front 31

Name the portion of the bronchioles

simple non-ciliated cuboidal cells and Clara cells;
alveoli open from one side

a. conducting bronchioles
b. terminal bronchioles
c. respiratory bronchioles
d. alveolar ducts

Back 31

c. respiratory bronchioles

Front 32

Name the portion of the bronchioles

no smooth muscle; alveoli open from all sides

a. conducting bronchioles
b. terminal bronchioles
c. respiratory bronchioles
d. alveolar ducts

Back 32

d. alveolar ducts

Front 33

what makes up the air-blood barrier

Back 33

Type I cell - basal lamina - capillary endothelium - rbc membrane

Front 34

Eupnea is Normal quiet breathing at rest. What is the normal number of breaths per minute

Back 34

8-16 breaths per minute

Front 35

Fill in the blank:

to low PaCO2 results
in respiratory ( acidosis/ alkalosis)
whereas too high of a PaCO2
results in respiratory (acidosis/alkalosis)

Back 35

to low PaCO2 results
in respiratory ALKALOSIS,
whereas too high of a PaCO2
results in respiratory ACIDOSIS

Front 36

too low PIO (e.g., at high altitude) and thus PaO results in which condition (hyperoxemia/ hypoxemia)

Back 36

hypoxemia

Front 37

t/f Composition of air changes as the altitude increases.

Back 37

false- Composition of air remains the same regardless of the altitude.

Front 38

t/f Partial pressure of inspired O2 decreases with increasing altitude.

Back 38

true- Fractional concentration of O2 remains at
0.21 regardless of altitude. Percentage of O2 saturation of arterial blood, however, decreases with increasing altitude.

Front 39

what is Dalton's Partial Pressure equation

Back 39

Pgas X = Fgas X • PB

Dalton's Law of partial pressures.
In a gas mixture, each specific gas will exert a pressure as if it alone occupied the entire
volume. The pressure exerted by the gas is proportional to its own concentration. To calculate
the partial pressure of a dry gas

Front 40

what does Boyle’s Law state

Back 40

At constant temperature, the volume of a given quantity of gas varies inversely with the
pressure to which that gas is exposed

chnique for pressure breathing is not unlike that used for intermittent positive pressure breathing in the clinic for
providing intermittent mechanical ventilation for purposes of augBoyle’s Law predicts that as pressure decreases (with increasing altitude) the volume
of gas in sealed cavities in the body will increase.

Front 41

what is Decompression sickness

Back 41

mostly nitrogen bubbles when breathing
air) can develop in the body of a diver, aviator or caisson worker whenever they
are exposed to a rapid reduction in barometric pressure (decompression).

Front 42

list names the layers of structures
that present a resistance to the diffusion of O2 as it passes from the alveolar gas into the RBC
traveling through a pulmonary capillary.

Back 42

1. fluid layer lining the alveolus (surfactant)
2. alveolar epithelium
3. interstitium
4. capillary endothelium
5. plasma
6. RBC membrane
7. RBC intracellular fluid

Front 43

Definition

Increased respiratory rate greater than 18 breaths / minute

Back 43

Tachypnea

Front 44

Definition

Increased ventilation that meets metabolic needs

Back 44

Hyperpnea

Increased respiratory rate (i.e. tachypnea) and/or overly deep breaths
e.g. during exercise

Front 45

Definition:
Increased ventilation that exceeds metabolic needs

Back 45

Hyperventilate-Increased respiratory rate (i.e. tachypnea) and/or overly deep breaths
e.g. during anxiety attack

Front 46

Definition:

Decreased respiratory rate less than 10 breaths / minute

Back 46

Bradypnea

Front 47

Defintion

Cessation of breathing

Back 47

Apnea

Front 48

Definition

Labored breathing

Back 48

Dyspnea

Front 49

what contributes mostly to the elasticity in the thorax

Back 49

Elastic due mainly to the joints of the ribs

Causes thoracic cavity to expand (opposes recoil of the lungs)

Front 50

List the muscle of normal respiration

Back 50

1. diaphragm

2. external intercostals

Front 51

Which muscles are used during forced inspiration

Back 51

1. diaphragm
2. external intercostal
3. Pectoralis minor
4. Sternocleidomastoid
5. Scalenes

Front 52

which muscles are used during forces expiration

Back 52

1. Internal intercostals
2. Obliques
3. Rectus abdominis

Front 53

which pleura Lines thoracic cavity and is attached to the diaphragm

Back 53

parietal pleura

Front 54

which pleura Covers lungs

Back 54

visceral pleura

Front 55

what is the pleura space

Back 55

Fluid-filled potential space between the pleural layers

Pressure in the space is less than pressure in the lungs (discussed later)

Due to recoil of lung and expansion of thorax

Allows lung to remain inflated

Front 56

in which zone is the Mucociliary escalator present

Back 56

conducting zone

Front 57

what is the effect of sympathetics on the smooth muscles of pulmonary tree? Which receptors are used to achieve this goal

Back 57

Sympathetics relax pulmonary smooth muscle (dilate bronchioles)

Via β2 adrenergic receptors

Front 58

what is the effect of parasympathetics on the smooth muscles of pulmonary tree? Which receptors are used to achieve this goal

Back 58

contract pulmonary smooth muscle (constrict bronchioles)

Via acetylcholine receptors (muscarinic receptors

Front 59

Describe the mucociliary escalator

Back 59

Goblet cells produce mucus which traps fine particulates (including pathogens)
Ciliated epithelial cells “beat” to propel particulates trapped in mucus to the pharynx

Front 60

what is the Anatomical dead space in the lungs? what is the volume of this space

Back 60

Conducting zone volume
Rule of thumb: volume in ml is equal to weight in pounds

e.g. 200 pound person has a 200 ml anatomical dead space

Front 61

what is Alveolar dead space? what is the volume in a normal health adult?

Back 61

Alveoli that do not participate in gas exchange
Due to lack of blood supply or damage to alveoli

Zero in normal, healthy individuals

Front 62

what is the Physiological dead space?

Back 62

Combination of anatomical and alveolar dead spaces

Front 63

Name the volume:

approximately 500 ml
Volume of air inspired or expired during normal, quiet breathing

Back 63

tidal volume

Front 64

Name the volume

approximately 3,000 to 3,300ml
Maximum amount of air that can be inspired at end of a normal inspiration

Back 64

Inspiratory reserve volume (IRV)

Front 65

Name the volume

– approximately 1,000 to 1,200ml
Maximum amount of air that can be expired at end of a normal expiration

Back 65

Expiratory reserve volume (ERV)

Front 66

Name the volume of air

cannot be measured with a spirometer (~ 1,200ml)
Volume of air remaining in the lungs after a forced expiration

Back 66

Residual volume (RV

Front 67

name the capacity

– approximately 2,200 to 2,400ml
Volume of air remaining in the lungs after a normal expiration

Back 67

Functional residual capacity (FRC)

FRC = ERV + RV

Front 68

name the capacity

– approximately 4,500 to 5,000ml
Volume of air forcefully expired from lungs after a maximal inspiration

Back 68

Vital capacity (VC)

VC = VT + IRV + ERV or VC = TLC – RV

Front 69

name the capacity

approximately 5,700 to 6,200ml
Volume of air in the lungs after a maximal inspiration

Back 69

Total lung capacity (TLC)

TLC = VT + IRV + ERV + RV

Front 70

Name the unit of rate for air flow

Volume of air forcefully expired after a maximal inspiration? What is the normal amount

Back 70

Normal FVC ≈ 5,000 ml

Front 71

Name the unit of rate for air flow

Volume forcefully expired in the first second? What is the normal value

Back 71

Normal FEV1 ≈ 3,500 to 4,000 ml

Front 72

Name the unit of rate for air flow

Volume forcefully expired in three seconds? What is the normal amount of air?

Back 72

Nearly the entire vital capacity (i.e. ~ 95% of)

Front 73

what is the formula for Helium Dilution Method to Measure FRC

Back 73

(C1) (V1) = C2 (V1 + V2)

Front 74

what is the formula for Boyle's Law? What does it state?

Back 74

Boyle’s Law: the product of pressure and volume is constant for a confined gas
P1V1 = P2V2

Front 75

Definition:

measure of how volume changes as a result of a pressure change ( delta Volume/ delta Pressure)

a. Compliance
b. Air Flow
c. Pressure
d. Resistance

Back 75

Compliance

Front 76

what is the normal compliance volume in the lungs

Back 76

Normal value of the lung is 0.13 liters / cm H2O

Front 77

what is Hysteresis

Back 77

a pathway, process or property in one direction differs from the pathway, process or property in the reverse direction

like the lung compliance curves

Front 78

At what point in the graph, is Recoil of lung and expanding force of chest wall equal each other

Back 78

When lung volume is at FRC

Front 79

At what point in the graph is Recoil of lung is decreased while expanding force of chest wall is increased

Lung and chest wall want to expand

Back 79

When lung volume is less than FRC

Front 80

when on the graph is Recoil of lung is increased while expanding force of chest wall is decreased

Lung and chest wall want to collapse

Back 80

When lung volume is greater than FRC

Front 81

why is normal lung compliance is dependent on surfactant

Back 81

Surfactant reduces surface tension (T)

Pressure (P) to keep alveoli inflated (i.e. collapsing pressure) is therefore very low

Allows alveoli to more easily remain inflated

Front 82

describe the pathogenesis of infant respiratory distress syndrome

Back 82

Lungs without surfactant

Surface tension is now very high

Collapsing pressures are now high, especially in smaller alveoli due to smaller radii (r)

Alveoli tend to collapse (type of atelectasis), especially smaller alveoli

Pressure gradients also produced from smaller alveoli to larger alveoli

Smaller alveoli collapse into larger alveoli

Front 83

how is Air Flow, Pressure and Resistance related

Back 83

Airflow= P1-P2/ R

R= 8vl/ Π r4

P1 = pressure at point 1 (e.g. of the alveoli)

P2pressure at point 2 (e.g. of the air we breathe)

ν = viscosity (e.g. of inspired air)

l = length

R= radius (e.g. of airways)

Front 84

what is the effects of sympathetics on the airway and resistance

Back 84

Sympathetics dilate airways (decreases resistance)

Front 85

what is the effects of parasympathetics on the airway and resistance

Back 85

Parasympathetics constrict bronchioles airways (increases resistance)

Front 86

what is the effect of High lung volume on resistance

Back 86

High lung volume (decreases resistance)

High lung volumes are associated with greater radial traction
i.e. airways are pulled open by interstitium
Increases radius and therefore decreases resistance

Front 87

what is the effect of low lung volume on resistance

Back 87

Low lung volume (increases resistance)

Low lung volumes are associated with less radial traction
i.e. airways not pulled open by interstitium
Decreases radius, even to the point of collapse

Front 88

Minute ventilation (VE) – volume of air moved into the airways per minute

what is the equation for minute ventilation

Back 88

VE = (VT) x (Respiratory Rate)

Front 89

Alveolar ventilation (VA) – volume of air moved into the alveoli per minute

what is the equation for alveolar ventilation

Back 89

VA = (VT – VD) x Respiratory rate

Front 90

ventilation requires pressure gradients. how are pressure gradients

Back 90

Pressure gradients created by changes in volumes (Ideal Gas Law)

Front 91

t/f Pleural pressure (Ppl), Pressure in the pleural cavity is always less than Palv. Why

Back 91

true-Aids in keeping the alveoli inflated
Produced by tendency of lungs to recoil and chest wall to expand

Front 92

t/f Transpulmonary pressure (Ptp) needs to be negative to keep the alveoli and airways inflated

Back 92

false- Transpulmonary pressure (Ptp) needs to be positive to keep the alveoli and airways inflated

Front 93

Describe the changes to the lungs during inspiration

Back 93

1. Contraction of respiratory muscles- Causes thoracic cavity to expand and thus pulls on the lungs via pleural membrane

Recoil of lungs is now increased- Ppl decreases toward -8 cm H2O, causing alveoli to inflate

Increases alveolar volume- Palv decreases toward -1 cm H2O (less than PB now)

Air rushes into lung down pressure gradient- Causes Palv to increase toward zero

Front 94

Describe what happens during expiration

Back 94

Relaxation of respiratory muscles

Decreases thoracic cavity volume toward resting (end of expiration) level-Recoil of lung decreases toward resting levels-
Ppl increases toward -5 cm H2O- Decreases alveolar volume toward resting levels

Palv increases above PB toward +1 cm H2O- Greater than zero due to greater air volume

Air rushes out of lung down pressure gradient- Causes Palv to decrease toward zero

Front 95

Describe the basis for how a pneumothorax develops

Back 95

Presence of air in the pleural cavity leading to an increase in Ppl
Ppl is no longer less than Palv
Causes the lung to collapse

Front 96

Describe the basis for how a pneumothorax develops

Back 96

Presence of air in the pleural cavity leading to an increase in Ppl
Ppl is no longer less than Palv
Causes the lung to collapse

Front 97

Describe the basis for how a pneumothorax develops

Back 97

Presence of air in the pleural cavity leading to an increase in Ppl
Ppl is no longer less than Palv
Causes the lung to collapse

Front 98

what is the difference between PaO2 and SaO2

Back 98

PaO2 = measures oxygen in the blood (80-100)

SaO2 = measures tissue perfusion (pulse ox >95%)

Front 99

What type of pnuemothroax? What causes this type of pneumo

Back 99

Simple pneumothorax means that air is allowed to enter and exit the pleural cavity

Causes equilibration of either Palv and Ppl or PB (and in essence, Palv) and Ppl

Ppl = Palv or PB = Ppl

this pic. pneumo from broken rib

Front 100

what type of pneumothorax? what causes this ?

Back 100

Tension pneumo

Air enters but does not exit the pleural cavity (air is trapped)

Causes a large increase in Ppl (Ppl > Palv)

Mediastinal structures are pushed to the opposite side of the thoracic cavity

Compresses the “unaffected” lung, the heart, and the great vessels

Unaffected lung is now “affected”

Decreases cardiac output

Front 101

which respiratory center ( dorsal or ventral) respiratory group?

Most active during inspiration

Some neurons also active during expiration

Primarily drive the diaphragm

Back 101

dorsal respiratory group

Front 102

which respiratory center ( dorsal or ventral) respiratory group?

Active during inspiration and expiration

Also contains pacemaker neurons (pre-Bötzinger complex)

Primarily drive the intercostals

Back 102

ventral respiratory group

Front 103

which center is responsible for the following in breathing ( apneustic or pneumotaxic- pontine) respiratory group

Not vital to the generation of respiratory rhythm

Helps regulate duration of inspiration

Causes longer inspiratory bursts

Causes long, deep inspiration

Back 103

apneustic respiratory group

Front 104

which center is responsible for the following in breathing ( apneustic or pneumotaxic- pontine) respiratory group

Not vital to the generation of respiratory rhythm

Helps regulate duration of inspiration

Causes shorter inspiratory bursts

Causes short, shallow inspiration

Back 104

pneumotaxic- pontine respiratory group

Front 105

Which portion of the breathing center is described by the following

voluntary aspect of breathing

Breathing is involuntary but can be voluntarily overridden

e.g. breath-holding or voluntarily hyperventilating

a. cerebrum
b. hypothalamus
c. chemoreceptors
d. diaphragm

Back 105

cerebrum

Front 106

which portion of the controlling of breathing does the following?

emotional aspect of breathing

e.g. increases respiratory rate during stress or excitement

Back 106

hypothalamus

Front 107

name the breathing control mechanism for the followig

Neurons in multiple areas of the medulla and pons

Play the biggest role in the regulation of breathing

Monitor the level of PCO2 / pH in arterial blood

a. cerebrum
b. hypothalamus
c. central chemoreceptors
d. lung stretch receptors

Back 107

c. central chemoreceptors

Front 108

name the breathing mechanism responsible for the following

Carotid body (glomus cells) in the the wall of carotid arteries

Monitor the level of PO2 (and to a lesser extent PCO2 / pH), in arterial blood

Oxygen stimulates breathing in extreme instances (PaO2 < 60 mm Hg)

a. cerebrum
b. hypothalamus
c. peripheral chemoreceptors
d. lung stretch receptors

Back 108

c. peripheral chemoreceptors

Front 109

which breathing mechanism Sends inhibitory impulse to brainstem when lungs are over-inflated

Back 109

lung stretch receptors

Front 110

according to Fick's Law:

Diffusion of gas across membrane is directly proportional to:

Back 110

VX = (D) (A) (P1 – P2) / ∆x

Diffusion coefficient (D)
Surface area (A)
Pressure gradient (P1 – P2)

Front 111

according to Fick's Law:

Diffusion of gas across membrane is inversly proportional to:

Back 111

Membrane thickness (∆x)

Front 112

what is the Physiologic shunt

Back 112

about 2% of cardiac output bypasses alveoli

Bronchial veins drain directly into pulmonary veins

Thebesian veins drain directly into left ventricle and left atrium

Front 113

how is Physiological Dead Space Volume (VD) estimated

Back 113

VD = VT X [(PaCO2 – PECO2)/ PaCO2 ]

Front 114

how is Alveolar Ventilation Equation calculated

Back 114

VA = ( VCO2 x K)/ PACO2

K = constant (863 mm Hg)
PACO2 = alveolar PCO2
VCO2 = rate of CO2 production

Front 115

how is Oxygen is transported in blood

Back 115

1. Dissolved

2. Hemoglobin

Front 116

how is Carbon dioxide is transported in blood

Back 116

1. Dissolved

2. Hemoglobin

3. Bicarbonate

Front 117

definition:

percent of Hb fully saturated with oxygen

a. SaO2
b. O2 capacity
c. O2 content

Back 117

a. SaO2

Front 118

definition:

greatest amount of O2 (in ml) that can be carried in 100 ml of blood

a. SaO2
b. O2 capacity
c. O2 content

Back 118

b. O2 capacity

Front 119

definition:

amount of O2 that is carried in 100 ml of blood

a. SaO2
b. O2 capacity
c. O2 content

Back 119

c. O2 content

Front 120

When each gram of Hb is fully saturated, it carries ___ ml of oxygen

Back 120

~ 1.36 ml of O2

Front 121

how how much O2 is extracted from blood by tissues

Back 121

approximately 5 vol % (20 vol % – 15 vol %) is extracted from blood by tissues

, 25% of O2 is extracted
from the blood by the tissues

Front 122

which shift Indicates a decrease in the affinity of Hb for O2

Back 122

Right shift- Hb releases O2 more readily

Front 123

which shift Indicates an increase in the affinity of Hb for O2

Back 123

left shift- Hb binds O2 more tightly

Front 124

which factors cause a right shift in the O2 – Hb binding curve

Back 124

↓ pH

↑ PCO2

↑ temperature

BPG

HBS

Front 125

which factors cause a left shift in the O2 – Hb binding curve

Back 125

Increase the Affinity of Hb for O2

↑ pH

↓ PCO2

↓ temperature

HbF

Methemoglobin

CO

Front 126

what is the double whammy of carbon monoxide poisoning

Back 126

CO displaces oxygen from hemoglobin

Hb has 250 times greater affinity for CO

Whatever oxygen is bound, is tightly bound

CO increases affinity of Hb for oxygen

Left shift
All of the above occurs while PO2 is unchanged

Front 127

what is the Haldane effect

Back 127

As more oxygen is bound to Hb, more CO2 will be released from Hb

Haldane effect (effect of oxygen on CO2 binding to Hb)

e.g. as occurs at the lungs

Front 128

how is CO2 transported at the tissue

Back 128

CO2 (produced during cellular respiration) enters red blood cell
CO2 hydrated (aided by carbonic anhydrase)
CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-
Accumulation of HCO3- causes diffusion to plasma
HCO3- exchanges for Cl- (chloride shift)
Hemoglobin aids in buffering the H+ also (Hb-H)

Front 129

how is CO2 transported in the lungs

Back 129

CO2 diffuses from red blood cells to alveoli
Causes HCO3- to combine with H+ to form more CO2
HCO3- + H+ ↔ H2CO3 ↔ CO2 + H2O
Decrease in HCO3- causes diffusion from plasma
Cl- exchanges for HCO3- (chloride shift)

Hemoglobin releases H+

Front 130

what is the difference between Diffusion-limited gas exchange and Perfusion-limited gas exchange

Back 130

Diffusion-limited gas exchange: the total amount of gas transported
across the alveolar-capillary barrier is limited by the diffusion process
As long as the partial pressure gradient is maintained,
diffusion will continue along the length of the capillary

Perfusion-limited gas exchange: the total amount of gas transported across the
alveolar-capillary barrier is limited by blood flow through the pulmonary capillary
The partial pressure gradient is not maintained and the only way to increase the amount of gas transported is by increasing blood flow

Front 131

which gas is used to demonstrate diffusion-limited gas exchange

Back 131

Carbon monoxide (CO) is a gas used to demonstrate diffusion-limited gas exchange

Front 132

which gas is used to demonstrate perfusion-limited gas exchange

Back 132

Nitrous oxide (N2O) is a gas used to demonstrate perfusion-limited gas exchange

Perfusion-limited gas exchange also occurs with O2 transport during normal conditions

Front 133

what is the difference is diffusion vs perfusion in the upper, middle and lower lobes of the lung

Back 133

Front 134

what is the effect of obstructive pulmonary disease on

1. ventilation
2. airway flow
3. TLC, FRC, RV

Back 134

Caused by airway obstruction
Decrease in ventilation
Decreases PaO2 (hypoxemia)
Increases PaCO2 (hypercapnia)
Impaired gas exchange can occur, Hypoxemia Hypercapnia

Changes in air flow
FEV1 is reduced due to obstruction
 FEV1 / FVC is greatly reduced

Hyperinflation of the lungs
Development of barrel chest in later stages

Front 135

name the obstructive disease

Loss of elastic fibers of airways and/or alveoli via proteases (especially elastase)

Loss of elastic recoil and thus an increase in lung compliance

Back 135

Emphysema

Front 136

in emphysema- which cells released Proteases and what is the effect of proteases

Back 136

mainly by neutrophils and macrophages in response to inflammation

Front 137

In which obstructive disease ( emphysema, bronchitis or asthma) does the following occur

Airways more prone to collapse (especially during forced expiration)

Breathe through pursed lips
Increases pressure within airways to keep them from collapsing

Back 137

emphysema

Front 138

what are 2 causes of emphysema

Back 138

1. Cigarette smoke increases release of proteases
2. AAT normally inhibits proteases from breaking down elastic fibers

Front 139

name the obstructive disease

Increased daily mucus production for at least 3 months in 2 or more consecutive years

Back 139

Chronic Bronchitis

Front 140

name the obstructive disease:

Hyperplasia and hypertrophy of goblet cells of the submucosa and thickening of mucosa

No damage to pulmonary capillary bed (therefore, perfusion is fine)

Back 140

Chronic Bronchitis

Front 141

name the obstructive disorder

1. Airway inflammation
2. Bronchoconstriction
3. Airway hyper-responsiveness

Back 141

asthma

Front 142

which type of pulmonary disorder this the following

FEV1 is reduced

However, FEV1 / FVC is normal or increased

FVC reduced relative to FEV1

Back 142

Restrictive Pulmonary Disease

Front 143

name the following restrictive lung disease

Inflammation to bronchioles and / or alveoli and / or pulmonary capillaries

Causes scarring and fibrosis

Lung becomes “stiff” (decrease in lung compliance

Back 143

Interstitial Lung Disease (ILD)

Front 144

Restrictive pulmonary disease can involve disease that affect the respiratory muscles. name 4 disease that would cause the following symptoms

Back 144

Amyotrophic lateral sclerosis / Lou Gehrig’s Disease
Guillain Barré
Myasthenia gravis
Muscular dystrophy

Front 145

name the restrictive lung disease

Immature respiratory system fails to produce surfactant

Decrease in lung compliance- Surface tension is now very high

Collapsing pressures are now high, especially in smaller alveoli - Atelectasis of alveoli (especially smaller alveoli)

Back 145

Infant Respiratory Distress Syndrome (IRDS)

Front 146

list 4 Adaptation to High Altitude / Hypoxemia

Back 146

1. Hyperventilation

2. Polycythemia

3. Increase in 2,3-biphosphoglycerate (BPG)

4. Pulmonary Vasoconstriction

Front 147

when will hyperventilation occur

Back 147

Will not occur unless PaO2 is less than 60 mm Hg

Stimulates peripheral chemoreceptors- Causes an increased level of expired CO2 (initial response)

Decrease in PaCO2 with a subsequent increase in arterial pH- Respiratory alkalosis

Inhibits central chemoreceptors
Decrease in ventilatory output

Front 148

what are the Compensatory mechanism in response to respiratory alkalosis

Back 148

Kidneys secrete (and thus excrete) HCO3-
pH returned to normal values (PaO2 is still low however)
Hyperventilation is allowed to resume

Front 149

t/f Hypoxemia causes the stimulation of erythropoietin release from kidneys

Back 149

true

Front 150

Acute Mountain Sickness (AMS) can be prevented with which drug and why

Back 150

Prevention with acetazolamide (Diamox)
Increases HCO3- excretion by the kidneys
Creates mild compensatory metabolic acidosis
Counteracts initial respiratory alkalosis

Front 151

why is Nifedipine used in High Altitude Pulmonary Edema (HAPE)

Back 151

Calcium channel blocker normally used to treat hypertension

Used to decrease increased pressure of pulmonary vasculature

Front 152

why is Dexamethasone used in High Altitude Cerebral Edema (HACE)

Back 152

Very powerful glucocorticoid
Used to decrease inflammation

Front 153

what are 6 benefits of hyperbaric oxygen therapy

Back 153

1. Greatly increases oxygen concentration in all body tissues

2. Stimulates angiogenesis to locations with reduced circulation

3. Improves blood flow to areas with arterial blockage

4. Stimulates an adaptive increase in superoxide dismutase

5. Powerful endogenous antioxidant

6. Aids the treatment of infection by enhancing neutrophil action

Front 154

Markus- PFT demo

Define the lung volume

volume of gas added to and then removed from the lungs with each breath

Back 154

tidal volume (VT)

Front 155

maximum volume of gas inhaled at the end of a spontaneous inspiration. It represents the lung’s reserve for increasing VT

Back 155

inspiratory reserve volume (IRV)

Front 156

maximum volume of gas expired at the end of a normal spontaneous expiration

Back 156

expiratory reserve volume (ERV)

Front 157

volume of gas left in the lungs at the end of a maximal expiration. It represents the minimum volume of gas that the lungs contain if both the lungs and thorax are intact;

Back 157

residual volume (RV

Front 158

t/f residual volume RV can be measured by spirometry

Back 158

RV cannot be measured via spirometry. In order to determine RV we must employ indirect methods

Front 159

what is the normal FEV1/FVC Ratio

Back 159

>70% of FVC

Front 160

what is the normal FEV3 / FVC ration

Back 160

>95% of FVC

Front 161

what is the FEV1/FVC Ratio in Obstructive airway disease

Back 161

less than 70%

Front 162

FVC ( Forced Vital Capacity) is a ( Volume or Flow) test

Back 162

FVC ( Forced Vital Capacity)
a VOLUME test

Front 163

FEV1 – (Forced Expiratory Volume in 1 second) is a ( Volume or Flow test

Back 163

FEV1 – (Forced Expiratory Volume in 1 second)
a FLOW test

Front 164

Describe the flow rates in obstructive vs restrictive

FEV1
FVC
FEV1/FVC
FRC
RV
TLC
compliance
PaO2
PaCO2

Back 164

OBSTRUCTIVE

FEV1-significantly ↓
FVC- ↓
FEV1/FVC- less than 80%
FRC- ↑
RV- ↑
TLC ↑ hyperinflation
compliance- ↑ loss of recoil
PaO2- ↓
PaCO2 - ↑
decrease pulmonary diffusing capacity ( DL )

loss of peripheral vascular elements on CXR due to loss of tissue

RESTRICTIVE

FEV1- ↓
FVC- ↓
FEV1/FVC- greater than 80%
FRC- ↓
RV- ↓
TLC ↓
compliance- ↓
PaO2- ↓
PaCO2 - ↑

Front 165

In asthma, maximum expiratory flows are ( increased or reduced) as measured by FEV1.

Moreover, TLC and FRC are ( increased or decreased) during episode

Back 165

In asthma, maximum expiratory flows are REDUCED as measured by FEV1.

Moreover, TLC and FRC are INCREASED during episode

Front 166

t/f weight is a factor in Normal Spirometric Values

Back 166

false- only a factor is severely obese

factors are
age
height
sex
race

Front 167

Reduced FEV1 indicates a flow abnormality of (obstruction or restriction)

Back 167

obstruction

Front 168

Reduced FVC indicates a volume abnormality of (obstruction or restriction)

Back 168

restriction

Front 169

Obstruction or Restriction

present when FEV1/FVC ratio is < 70%

Back 169

Obstruction

Front 170

Obstruction or Restriction


(often) present when FEV1/FVC ratio is > 80%
(But may be normal)

Back 170

Restriction

Front 171

t/f in restrictive lung diseases volumes are increased, but flow rates are normal or increased

Back 171

false- Volumes are DECREASED, but flow rates are normal or increased

Front 172

restrictive lung disease can be due to: Parenchyma, chest wall , diaphragm

Parenchymal diseases
have numerous etiologies, and are referred to as interstitial lung diseases (ILD)

what are the common features of ILD (3)

Back 172

1. decreased lung compliance

2. decreased lung volumes

3. diffusion (DL) at the alveolar-capillary membrane is impaired (or decreased DLco)*

Front 173

In obstructive lung disease is the airway narrowing during ( inspiration or expiration)

Back 173

KNOW!!

during EXPIRATION

obstructs or limits outflow of air from lungs

Both flow rates and volumes are affected

Front 174

List 4 Mechanisms of Obstruction in Disease

Back 174

1. Chronic Bronchitis - blue bloaters

2. Emphysema - pink puffers

3. Asthma

4. Bronchiectasis

Front 175

name the obstructive disease and the findings

spasmodic contraction of smooth muscle in the bronchi

Back 175

asthma

cough, wheezing, dyspnea, tachypnea, hypoxemia, pulsus paradoxus, mucus plugging

reversible bronchoconstriction from hyperresponsiveness

Front 176

name the obstructive disease and the findings

an inflammatory condition of the bronchi, which results in the excessive production of mucus

Back 176

Chronic Bronchitis - blue bloaters

productive cough for more than 3 consecutive months in 2 years. disease of small airway

Front 177

name the obstructive disease and the findings

enlargement of air spaces and loss of lung recoil resulting destruction of lung alveolar wall

Back 177

Emphysema - pink puffers

increase elastase activity, increase lung compliance due to loss of elastic fibers.

pts exhale through pursed lips to increase airway pressure and prevent airway collapse during exhalation

centriacinar- from smoking

panacinar-alpha 1 antiprotease deficiency or liver cirrhosis

paraseptal-from bullae which can rupture and cause spontaneous pneumothorax, in you healthy males

Front 178

t/f In asthma both inflow and outflow limited due to bronchoconstriction throughout respiration, but the pattern on PFTs is that of obstruction

Back 178

true -

Front 179

name the obstructive disease

Epithelial cells exhibit abnormal Cl- transport resulting in viscous mucus in the airways with impaired mucociliary clearance; recurring respiratory infections destroy the cellular constituents of the airways resulting in irreversible obstruction to airflow

Back 179

cystic fibrosis

Front 180

emphysema, anemia*, restrictive diseases, pneumonectomy, pulmonary hypertension*, and recurrent pulmonary emboli*

will have (low or high) Diffusion Test (DLCO)

Back 180

low

Front 181

The amount of gas in the lungs depends on which 2 factors

Back 181

1. activity of the respiratory muscles

2. mechanics of the Lung Chest wall system (L-CW)

Front 182

which 2 methods can be used to measure FRC

Back 182

Helium dilution
Body plethysmograph

*FRC = ERV + RV

Front 183

RV (increases or decreases) with obstructive lung disease and (increases or decreases) with restrictive lung diseases

Back 183

RV INCREASES with obstructive lung disease and DECREASES with restrictive lung diseases

Front 184

Anesthetic Lecture: Koerker

Preanesthetic Medications include which groups of med

Back 184

1. Sedatives

2. Analgesics

3. anticholinergic muscarinic blockers (atropine) to dry secretions & reduce reflexes

Front 185

list the Stages of Anesthesia

Back 185

1 analgesia

2. excitement

3. surgical anesthesia

4. medullary depression

Front 186

what leads to the Neuropharmacological Basis for Stages of Anesthesia

Back 186

- due to differential sensitivity of specific neurons or neuronal pathways to the anesthetics

Front 187

What causes Stage I (Analgesia) in the Stages of Anesthesia

Back 187

an interruption of sensory transmission in the spinothalamic tract, including nociceptive (painful) stimuli. This interruption occurs because the cells in the substantia gelatinosa in the dorsal horn of the spinal cord are very sensitive to a relatively low concentration of anesthetic in the central nervous system.

Front 188

what causes Stage II (Excitement), seen only with diethyl ether,

Back 188

resulted in irregular respiration, coughing, dilated pupils, and marked eye movements. Due in part to irritation of respiratory mucosa and release of catecholamines. Occurs with higher, disinhibitory concentrations of anesthetic, resulting in blockade of many small inhibitory neurons such as Golgi type II cells. A paradoxical facilitation of excitatory neurotransmitters also occurs

Front 189

what causes Stage III (Surgical Anesthesia)

Back 189

progressive depression of ascending pathways in the reticular activating system. In addition, the suppression of spinal reflex activity contributes to the muscle relaxation that is produced by some agents in this stage of anesthesia

Front 190

what causes Stage IV (Medullary Depression)

Back 190

observed only at toxic doses of anesthetic when cardiorespiratory collapse occurs. Fortunately, neurons in the respiratory and vasomotor centers of medulla are relatively insensitive to the effects of the general anesthetics. It is speculated that regional variations in anesthetic actions may correspond to regional variations in subtypes of the GABAA receptor.

Front 191

name the stage in the anesthetic pathway

Minimal CNS depression

Some amnesia along with analgesia

Respiration and pupils normal

No eye movement or loss of reflexes


a. analgesia
b. excitement
c. surgical anesthetic
d. medullary depression

Back 191

analgesia

Front 192

name the stage in the anesthetic pathway

Sensory transmission of nociceptive (painful) stimuli in spinothalamic tract are interrupted due to depression of substantia gelatinosa in dorsal horn of spinal cord

a. analgesia
b. excitement
c. surgical anesthetic
d. medullary depression

Back 192

analgesia

Front 193

name the stage in the anesthetic pathway

Due to inhibition of inhibitory neurons (e.g. Golgi type II cells) & release & paradoxical facilitation of catecholamines

a. analgesia
b. excitement
c. surgical anesthetic
d. medullary depression

Back 193

excitement

Front 194

name the stage in the anesthetic pathway

Respiration – very irregular, coughing

Pupils dilated

Eye movements marked

Loss of eyelid (blink) reflex

a. analgesia
b. excitement
c. surgical anesthetic
d. medullary depression

Back 194

excitement

Front 195

name the stage in the anesthetic pathway

Respiration normal and regular

Pupils normal

Diminishing eye movements to fixed stare

Loss of swallowing, conjunctival and pharyngeal reflexes

a. analgesia
b. excitement
c. surgical anesthetic
d. medullary depression

Back 195

c. surgical anesthetic

Front 196

name the stage of anesthesia

Depth of expiration decreases

Pupils dilate and won’t respond to light

Loss of carinal reflex

Can rapidly progress to Stage IV unless action is taken to decrease depth of anesthesia & stress

Back 196

stage 3: surgical anesthesia

Front 197

name the stage of anesthesia

Cardio-respiratory collapse due to depression of respiratory and vasomotor centers of medulla. Fortunately, neurons are relatively insensitive to depressant effects of GA.

Back 197

stage 4: medullary depression

Front 198

name the stage of anesthesia

Fixed, dilated pupils = signs of pending coma or death

Back 198

stage 4: medullary depression

Front 199

what is the Induction Phase of anesthesia

Back 199

Time to reach plane 3 of stage III. The shorter, the better.

Front 200

how can the induction phase of anesthesia be shortened

Back 200

Induction is shortened by hyperventilating (with ventilation-limited (diffusion-) GAs (eg. halothane with high B/G part. coef.), decreasing cardiac output (allows pp to ), in children (high resp. rate)or patients in shock ( CO & vent. ppalv,) or with thyrotoxicosis (high resp. rate).

Front 201

t/f Agents that are very soluble in the blood (e.g., nitrous oxide) show rapid induction and recovery.

Back 201

false- Agents that are POORLY soluble in the blood (e.g., nitrous oxide) show rapid induction and recovery.

Front 202

t/f . Agents that are poorly soluble in the blood (e.g., halothane) have prolonged induction and recovery

Back 202

false- . Agents that are HIGHLY soluble in the blood (e.g., halothane) have prolonged induction and recovery

Front 203

The more soluble an anesthetic is in the blood, the ( lower or higher) will be the coefficient, and the longer will be the induction and recovery periods

Back 203

The MORE soluble an anesthetic is in the blood, the HIGHER will be the coefficient, and the LONGER will be the induction and recovery periods

Front 204

what is the Maintenance phase of anesthesia

Back 204

period where the administration of the anesthetic agent is kept at the right level to accommodate the surgical procedure

Front 205

what is the Recovery phase of anesthesia

Back 205

reverse of induction (there is a decreasing concentration
of the anesthetic agent)

Front 206

The more soluble an agent is in blood, the (shorter or longer) the time required for equilibrium to be established between the pulmonary phase and the circulatory phase

Back 206

The MORE soluble an agent is in blood, the LONGER the time required for equilibrium to be established between the pulmonary phase and the circulatory phase

Front 207

Describe the following as either Ventilation (diffusion) -limited anesthetics or Perfusion-limited anesthetics and give examples

Have slow, rate limiting equilibration of alveolar with inspired partial pressures.

Results in slow induction and slow recovery.

Can speed up induction by increasing rate of rise of alveolar partial pressures

Back 207

Ventilation (diffusion) -limited anesthetics (e.g. diethyl ether, enflurane, isoflurane, halothane)

Front 208

Describe the following as either Ventilation (diffusion) -limited anesthetics or Perfusion-limited anesthetics and give examples

Induction and recovery occur quickly.

Agents that are less soluble in blood, induce anesthesia faster

Back 208

Perfusion-limited anesthetics (e.g. nitrous oxide, desflurane, sevoflurane)

Front 209

75% of cardiac output/min. goes to organs representing 10% of body mass. list the organs

Back 209

brain, liver, kidneys, heart, lungs

Front 210

Potency of general anesthetic is directly related to which component of the general anesthetic

Back 210

Potency of GA is directly related to its lipid solubility.

More potent GAs require lower concentrations to produce anesthesia

Front 211

t/f MAC is directly related to anesthetic potency

Back 211

false- MAC is INVERSLEY related to anesthetic potency

The higher the potency, the lower the MAC)

Front 212

what is Minimum alveolar concentration, MAC

Back 212

is an attempt to determine the true potency of an anesthetic agent.

The MAC is the percent alveolar concentration at one atmosphere pressure at which 50% of patients will not respond to a skin incision, i.e., ED50

Front 213

what is the major route of elimination for a general anesthetic

Back 213

exhalation

Exhalation of GA with low blood:gas partition coefficients (e.g. nitrous oxide or desflurane) is so rapid, back diffusion from blood to alveoli, displaces air from alveoli, leading to diffusion hypoxia. Prevent by ventilating with O2 after terminating GA

Front 214

match the blood gas coefficient with its respective anesthetic

halothane or nitrous oxide

0.47 or 2.30

Back 214

halothane = 2.30 MAC=.75 long onset and slow recovery

nitrous oxide= 0.47 MAC >100 rapid onset and recovery

Front 215

t/f GAs excite excitable tissue.

Back 215

false- GAs DEPRESS excitable tissue.

Front 216

t/f GAs depress frequency of EEG.

Back 216

true

Front 217

t/f GAs increase metabolic rate of brain.

Back 217

false- GAs decrease metabolic rate of brain.

Front 218

what is the Effects of general anesthesia on Respiratory System (4)

Back 218

1. Tonic stimulation by reticular activating system to respiratory center is lost. Therefore, respiratory center loses its drive to increase ventilation during hypoxia.

2. Respiratory Center is depressed.Sensitivity to changes in CO2 is reduced.
Consequently, partial pressure of CO2 in arterial blood increases.

3. Amplitude of respiration is depressed resulting in decreased tidal volume

4. Mucociliary function in airways is depressed leading to pooling of mucus, atelectasis, and respiratory infections

Front 219

t/f GAs cause CV changes by depressing the integrative functions of the CNS

Back 219

true

Front 220

is the heart itself is directly affected by anesthetic agents.

Back 220

Yes, The heart itself is directly affected by anesthetic agents. Anesthetics may effect the CVS by acting on the central nervous system, acting on the heart muscle itself, on cardiovascular smooth muscle and/or on other aspects of the vascular system

Front 221

t/f Halogenated GAs sensitize the myocardium to cardiac arrhythmias, especially in presence of elevated levels of catecholamines.

Back 221

true called catecholamine sensitization

Front 222

which catecholamines sensitize the myocardium to anesthetic effects

Back 222

epinephrine or norepinephrine. Halogenated anesthetic agents are most likely to produce this sensitization.

Front 223

what are the Effects of general anesthetics on the Renal System

Back 223

1. decrease urinary output due to:

2. Decreased BP

3. Vasoconstriction within kidney

4. Central stimulation of anti-diuretic hormone

Halogen radical metabolites of some GAs may be directly nephrotoxic (e.g. Sevoflurane)

Front 224

what are the Effects of general anesthetics on the liver function

Back 224

All inhalation GAs decrease hepatic blood flow by 15-45%

Front 225

what is the effect of Halogenated hydrocarbon GAs on the uterine smooth muscle

Back 225

Halogenated hydrocarbon GAs RELAX the uterine smooth muscle

Front 226

what is the most commonly used anesthetic for children in U.S. because of low incidence of adverse effects

Back 226

Halothane (Fluothane®)

Front 227

which anesthetic can be Secondary Rx for status asthmaticus

Back 227

Halothane (Fluothane®)

Front 228

what is the risk of using Halothane (Fluothane®) during delivery of a baby

Back 228

Causes uterine relaxation which is helpful in manipulating and positioning fetus for delivery BUT may lead to INCREASE blood loss after caesarean section or therapeutic abortion

Front 229

what are Halothane's adverse effects (5)

Back 229

1. Respiratory Depression

2. Profound myocardial depression

3. Poor analgesia

4. Hepatotoxicity

5. malignant hyperthermia

Front 230

what is the inheritance patter of Malignant Hyperthermia and the genetic defect behind the condition

Back 230

autosomal dominant characteristic linked to chromosome 19 which effects ryanodine receptor in sarcoplasmic reticulum Ca++ channel.

Halothane incriminated more than other GAs

Front 231

what are the warning signs of Malignant Hyperthermia

Back 231

1. Myopathy or neuropathy

2, Muscle spasms and pain

3.Elevated serum creatinine phosphokinase

Front 232

what is the Prodromal sign of malignant hyperthermia

Back 232

Prodromal sign = muscle hypertonus in masseter muscle in response to succinylcholine

Front 233

what is the population that malignant hyperthermia is usually seen

Back 233

Risk absent < 3 yo, peak at 20 yo

Predominantly in muscular males

Front 234

what is the treatment for malignant hyperthermia (5)

Back 234

1. Quickly cool body

2. Use sodium bicarbonate to correct acidosis

3. Administer O2

3. Correct hyperkalemia with insulin and glucose

3. Specific antidote = procaine or procainamide

4. iv mannitol is used to clear myoglobin from kidneys.

5. Dantrolene, a central acting muscle relaxant that blocks calcium release from sarcoplasmic reticulum, is used to relieve muscle hypertonus

Front 235

Isoflurane is pre-eminent GA for adults in U.S. even though costs 25X more than halothane.

Isoflurane is :Non-flammable

Better muscle relaxant than enflurane

Less respiratory depression than enflurane

Less depression of cardiac output (CO) than enflurane or halothane

what is the major adverse effect of using Isoflurane

Back 235

May cause coronary steal and worsen angina in patients with ischemic heart disease

Front 236

which anesthetic has Closest to ideal inhalation anesthetic and why

Back 236

Sevoflurane (Ultane®)

Pleasant odor provides useful alternative to halothane in children

Popular for outpatient anesthesia due to rapid smooth induction and rapid recovery

Does not produce tachycardia-Therefore, preferable in patients with myocardial ischemia

Most effective bronchodilator among inhalation GAs

Front 237

why are Barbiturates Contraindicated in patients with acute intermittent porphyria

Back 237

1. Induces hepatic ALA synthase

2. Effects liver microsomes

3. Aggravates porphyria

Front 238

Elder Microbiology

what is the infection that is the leading cause of death world wide

Back 238

acute LRTI

Front 239

what is the leading cause of community acquired pneumonia, follwed by #2 and #3

Back 239

the most common cause of CAP,

#2 Haemophilus influenzae

#3 atypicals, Mycoplasma pneumoniae, Chlamydia pneumoniae, and Legionella

Front 240

which drug is recommended in as an antibiotics for community acquired pneumonia in a pt who was previously healthy with no use no use of antibiotics in the past 3 months

Back 240

macrolide (MACE)

Front 241

which drugs are recommended in as an antibiotics for community acquired pneumonia in a pt who has comorbities such as CHF, diabetes, renal dysfunction, alcholism or use use of antibiotics in the past 3 months

Back 241

give respiratory fluoroquinolones

or beta-lactam + macrolide

Front 242

what are the major criteria for community acquired pneumonia

Back 242

invasive mechanical ventilation

septic shock with the need for vasopressors

Front 243

what are 4 minor criteria for community acquired pneumonia

Back 243

respiratory rate >30

PaO2/FiO2 <250

multi-lobar infiltrates

confusion/disorientation

Front 244

if Pseudomona Aeroginosa is suspected in community acquired pneumonia what is the treatment

Back 244

beta-lactams (pippercillin+tazobactam, cefepime)

or beta-lactam + aminoglycosie +azithromycin

or eta-lactam + aminoglycosie +fluoroquinolone

Front 245

t/f most Hospital Acquired Pneumonia is from staff not washing their hands

Back 245

false- 80%-90% are ventilator related

Front 246

what are the risk factors for multi-drug resistance in ventilator acquired pneumonia

Back 246

1. previous antimicrobial therapy

2. currently hospital stay or ICU

3. high frequency of mutli-drug resistance in community

4. risk factors for hospital acquired pneumonia

Front 247

what is the antibiotic of choice for a pt with hospital acquired pneumonia with Step pneumo or H. Influenza with early onset and no previous illness or antimicrobial use and not know to be MDR

Back 247

Ceftrioxone

Front 248

definition

refers to pneumonia that occurs prior to hospitalization with specific risk factors
immunosuppression
recent hospitalization
residence in a nursing facility
need for dialysis

Back 248

Healthcare Associated Pneumonia

Front 249

Amphotericin B- is lipophilic
binds to ergosterol/cholesterol

What are the adverse effects of Ampho B

Back 249

nephrotoxicity
hypokalemia
hypomagnesaemia
anemia
renal tubular acidosis

Front 250

Ampho B, is useful for treating which life-threatening, progressive fungal infections

Back 250

aspergillosis
cryptococcus
histoplasmosis

Front 251

which azole has >90 oral bioavailability and is renally excreted

Back 251

Fluconazole

Front 252

t/f Fluconazole covers all fungus

Back 252

false- does NOT cover Aspergillus

Front 253

Which 2 azoles coverall the major fungi such as Aspergillus ,Histoplasma , Coccidioides , Blastomyces and Sporothrix

Back 253

Itraconazole and Voriconazole

Front 254

what are the AEs of VORICONAZOLE

Back 254

alterations in visual perception ~30%
blurring, color discrimination, photophobia
if Rx > 28 d, then must test visual acuity, visual fields, and color perception

pregnancy category D

Front 255

list the Echinocandins

Back 255

anidulofungin

caspofungin

micafungin

Front 256

what is the mechanism of action for Echinocandins

Back 256

cell wall inhibitor
1,3--D glucan
cell wall target absent from mammalian cells

Front 257

what is the treatment for Aspergillus

Back 257

lipid ampho-B itraconazole
caspofungin posaconazole
voriconazole

Front 258

what is the treatment for Histoplasmosis

Back 258

itraconazole lipid ampho-B

Front 259

what is the treatment for Blastomycosis

Back 259

itraconazole lipid ampho-B

Front 260

what is the treatment for Crytpococcosis

Back 260

fluconazole lipid ampho-B

Front 261

what is the treatment for coccidioidomycosis

Back 261

fluconazole lipid ampho-B
posaconazole

Front 262

what is the treatment for mould or Fusarium

Back 262

voriconazole lipid ampho-B

Front 263

what are the first line of drugs for Tb

Back 263

RIPES

rifampin (RIF)
isoniazid (INH)
pyrazinamide (PZA)
ethambutol (ETH)
streptomycin

Front 264

what is the mechanism of action for isoniazid (INH) and how is it metabolized

Back 264

disrupts cell wall formation by inhibition of mycolic acids, bactericidal, active against intracellular and extracellular organisms
penetrates into phagocytes

hepatic metabolism, rate of metabolism is genetically determined

Front 265

what is the mechanism of action of rifampin

Back 265

inhibits RNA synthesis by binding to DNA-dependent RNA polymerase

Front 266

what are the AE of ethambutol

Back 266

optic neuritis-
loss of visual acuity
red-green color blindness

Front 267

which aminoglycoside is used in the treatment of Tb and what is its mechanism of action

Back 267

streptomycin

inhibits protein synthesis at the 30s subunit

Front 268

what other conditions (other than Tb) can streptomycin be used for

Back 268

tuberculosis
plague
tularemia

Front 269

what are the AEs of streptomycin

Back 269

Aminoglycosides:

nephrotoxicity
ototoxicity
neuromuscular blockade

Front 270

which drug is used for the following and what is its mechanism of action

Herpes simplex (HSV) pneumonia

Herpes varicella-zoster (HVZ) pneumonia

Back 270

acyclovir-inhibits DNA synthesis
irreversibly binds to DNA complex terminating replication

Front 271

which drug is used for the following and what is its mechanism of action

Respiratory Syncytial Virus (RSV)
default setting for other respiratory viruses
measles pneumonitis
hantavirus pulmonary syndrome
SARS

Back 271

ribivarin-by inhibits
viral mRNA, viral RNA dependent RNA polymerase and
interferes with guanine triphosphate synthesi

Front 272

which drug is used for Influenza A as a treatment and prophylaxis. what is its mechanism of action

Back 272

amantidine and ramantadine- inhibit viral mRNA disrupting RNA synthesis

Front 273

which influenza A and B drug is inhaled and which one is oral. ( zanamivir and oseltamivir)

what is their mechanism of action

Back 273

zanamivir is inhaled- no systemic absorption
renal excretion. AE bronchospasm and cough


oseltamivir is PO- good oral absorption and activated in liver, also renal excreted

both are neuramidase inhibitors

Front 274

Name the virus:

Nonenveloped, ss (+) RNA, preferes to grow at 33C, Binds to ICAM-1 on nasal epithelium to trigger cytokines and inflammatory process, peaks in fall and and spring. most common cause of common cold

a. Rhinovirus
b. Coronavirus
c.Adenovirus
d. Coxsackie A virus

Back 274

Rhinovirus

Front 275

Name the virus:

enveloped, ss (+) RNA, preferes to grow at 33C, replicates in ciliated epithelium o trigger cytokines and inflammatory process, peaks in winter and and spring. Second most common cause of common cold

a. Rhinovirus
b. Coronavirus
c.Adenovirus
d. Coxsackie A virus

Back 275

Coronavirus

Front 276

Name the virus:

nonenveloped, ss (+) RNA, Bind to ICAM-1, early replicaiton in lymphoid tissue . Lytic virus
antibody formation most important protective response against reinfection. prevalent in summer and also causes Herpangina
a. Rhinovirus
b. Coronavirus
c.Adenovirus
d. Coxsackie A virus

Back 276

d. Coxsackie A virus

also causes Hand-foot-and-mouth disease

Front 277

Name the virus:

nonenveloped, ds (+) DNA, preferes to grow at 33C, • Lytic virus – results in cell death, causes pharyngitis, acute respiratory disease in military recruits

a. Rhinovirus
b. Coronavirus
c.Adenovirus
d. Coxsackie A virus

Back 277

Adenovirus

Front 278

what is the most probably source of this pulmonary thomboembolus and what are the risk factors for developing this thromboembolus

Back 278

Majority (95%) originate in the femoral vein

Stasis of blood flow (e.g., prolonged bed rest), hypercoagulable states

Front 279

what determines the pulmonary vessels that are occuluded

Back 279

Size of the embolus determines pulmonary vessel that is occluded.

Large emboli occlude the major vessels (saddle embolus)

Small emboli occlude medium-sized and small pulmonary arteries.

Front 280

Chapter 8 notes and TL #1

Cancers of the lung, head and neck present with which symptoms

Back 280

Present with dyspnea, weight loss, abnormal weakness or neurologic
symptoms coupled with abnormal mass, adenopathy , percussion or
lung sounds helps to differentiate between neoplastic tumors and
other disease

Front 281

t/f Lung cancer is the Leading cause of cancer death, and the leading cause of cancer death in women since 1987

Back 281

trud

Front 282

what are the risk factors for lung cancer

Back 282

Smoking
• Obstructive lung disease
– Worse spirometry = greater risk
• Passive smoke
• 1st degree relative with lung cancer
• Pulmonary Fibrosis → linked to “scar carcinoma”
• Air pollutants
• Radon
• Other: asbestos, arsenic, nickel, hydrocarbons, radiation

Front 283

Asbestos causes mesothelioma . Is there an increased risk of mesothelioma with asbestos/smoking combination

Back 283

No increased risk

Front 284

rank the lung cancers in order from most frequent to least frequent

Back 284

most frequent-
– Adenocarcinoma (30%) peripheral- early mets, Hypertrophy Pul Osteo, DIC

– Squamous cell carcinoma (25%+)-central. obstruction, cavitation, late mets, superior sulcuc, hypercalcemia, clubbing

Small cell carcinoma (25%)- early mets, SIADH, Eaton Lambert

Large cell carcinoma (15%)- peripheral . early mets, clubbing

– Bronchioalveloar (5%) - bronchorrhea- non-smokers' lung cancer

• Other (endocrine and pleural derivatives) Rare.
– Carcinoid
– Mesothelioma

Front 285

where is adenocarcinoma usually located in the lung

Back 285

periphery

Front 286

why is the considered non-smokers lung

Back 286

Women frequently affected
• Peripheral (75%)

• Aggressive metastases
– Well-differentiated
– Alveolar bronchial and lymphatic spread

– mistaken for “the unresolving pneumonia”

• Most present as SOLITARY PULMONARY NODULE

• Sputum cytology, low yield without cough/hemoptysis

• Clubbing/hypertrophic pulmonary osteoarthropathy more common than in squamous cell carcinoma

• Chemo- and radiation therapy response poor

Front 287

which lung cancer has the best prognosis. how does this cancer present. In what patient population is this found

Back 287

multifocal bronchoalveolar

1 yr survival >80% after resection
• DIFFUSE form survival is poor: median < 6 mos
• Bronchorrhea (copious sputum production) present in 20%
• Most likely form to find in NON-SMOKER

Front 288

Is squamos cell carcinoma (central of peripheral) .

Is there an association with smoking

list 5 characteristics

Back 288

strong association with smoking

prevalence =25%+

Obstruction
Cavitation
Late metastases
Superior sulcus
Hypercalcemia
Clubbing

Front 289

where is large cell carcinoma located (central or peripheral) which other lung cancer is located peripherally

what other conditions are associated with this type of CA

what is the treatment

Back 289

peripheral- along with adenocarcinoma

Aggressive metastases
• Clubbing and pulmonary osteoarthropathy common (but <adenocarcinoma)
• Growth more rapid than adenocarcinoma
• Treatment by surgery

Front 290

where is small cell carcinoma usually located (central or peripheral)- what other CA also located here

list the defining features

is this associated with smoking

what other conditions are associated with small lung CA

what is the treatment

Back 290

central- also squamous

80% hilar/perihilar location
• Smokers & titanium miners
• Non-surgical treatment only
• Paraneoplastic Syndromes are prominent, including
• -SIADH
- ACTH production
- Lambert-Eaton (Myasthenic) Syndrom

Front 291

what other conditions are associated SVC syndrome

Back 291

SPHERE of complications in lung Ca

SVC syndrome
Pancost tumor
Horner's (PAM)
Endocrine problems
Recurrent laryngeal
Effusions (pleural and pericardial)

Front 292

“PARANEOPLASTIC” SYNDROMES include

SIADH- what is this

Back 292

SIADH- small cell (ADH excess leads to water retention which leads to hyponatremia)

Front 293

what other paraneoplastic syndromes are seen with lung cancer

Back 293

Increased ACTH- Small cell, Bronchial carcinoid- (hypokalemia, muscle weakness)
• Hypercalcemia- Squamous cell, carcinoid
• Calcitonin- (hypocalcemia) small cell, adenocarcinoma
• Gynecomastia-(Increased FSH)-large cell, adenocarcinoma

Front 294

what is the TNM system of staging cancers

Back 294

TNM SYSTEM (Tumor, lymph Nodes, Metastases

Front 295

TL #2 ARDS

Define ARDS by 4 clinical criteria: 3 positive features and one exclusion criterion.

Back 295

1. new bilateral infiltrates and Severe respiratory distress (without CHR)and 1 or more risk factors
(including infection, aspiration, pancreatitis, and trauma)

2.Impaired arterial oxygenation (hypoxemia)

3. Bilateral pulmonary infiltrates on chest radiograph

4. No clinical evidence of elevated left atrial pressure (or pulmonary artery occlusion pressure of < 18mmHg)

Front 296

what is the he cardinal feature of ARDS, and what causes it

Back 296

refractory hypoxemia, caused by protein rich alveolar edema after damage to the integrity of the lungs capillary-alveolar barrier

Front 297

what is the effect of Widespread alveolar flooding in ARDS (3)

Describe the effect on compliance, V/Q, and shunting

Back 297

1. impairs alveolar
ventilation,

2. excludes oxygen,

3. inactivates surfactant;

this, in turn, decreases lung compliance, increases
dispersion of ventilation and perfusion, and produces
INTRApulmonary shunt.

Front 298

how can an intrapulmonary shunt be found

Back 298

when hypoxemia does not
improve despite oxygen administration

hypoxemia in ARDS does respond to positive end-expiratory pressure,

Front 299

what are the most common causes of ARDS

Back 299

1. sever infection( sepsis, pneumonia)

aspiration, trauma, pancreatitis, several blood transfusions, smoke or toxic gas inhalation, and certain types of drug toxicity

Front 300

Define acute lung injury (ALI) and ARDS by ratios of pulmonary gas exchange.

Back 300

ALI- A PaO2-FiO2 of 300 or less. (ALI- hypoxemia + pulmonary infiltrates WITHOUT elevated left atrial pressures) decreased lung compliance

ARDS- PaO2-FiO2 of 200 or less regardless of the amount to fPEEP needed to support oxygenstion

Front 301

Describe 3 aspects of pathophysiology in ARDS, regardless of cause: cell types damaged, histopathologic features in acute phase, and effect on PaO.

Back 301

Acute exudative phase
1. damage involves both the endothelial and epithelial surface and disrupts the lung's barrier function--> flooding alveolar spaces with fluid--> inactivating surfactant--> inflammation--> severe gas Xchange abnormalities and loss of lung compliance =bilateral infiltrates

findings-
1. diffuse alveolar damage, including capillary injury, and areas of exposed alveolar epithelial basement membrane
2. alveolar spaces are lined with hyaline membranes and are filled with protein-rich edema fluid and inflammatory cells. The interstitial spaces, alveolar ducts, small vessels,and capillaries also contain macrophages, neutrophils, and RBCs

Decrease in PaO2 as there is an increase in lung water and pulmonary artery pressure

Front 302

Identify 4 cell types that are activated and 3 biochemical sequthe development of edema and hyaline membranes in ARDS.

Back 302

1.a. endothelial activation, and adhesion molecule expression
b. fibroblast activation
c. neutrophil activation and migration
d. alveolar macrophage activation

2. a. activation of coagulation,
b. inhibition of fibrinolysis
c. inactivation of surfactant
d. hyaline membrane deposit

Front 303

Describe pathophysiologic sequelae when the acute (exudative) phase of ARDS
progresses to the fibrosis (proliferative) phase.

Back 303

progress to a fibrosis with persistent hypoxemia, increased dead space pulmonary hypertension, and further loss of lung compliance.

CT may show often shows diffuse interstitial thickening and blebs or honeycombing. Pathologic examination of the lung shows fibrosis with collagen deposition, acute and chronic inflammation, and incomplete resolution of edema

Front 304

Explain how the immune response to sepsis produces inflammation in ARDS.

Back 304

Activation of innate responses generates the inflammatory mediators of ARDS.

1. Innate immunity provides the first-line host defense against pathogens-identifies certain patterns of cell activation; so only needs, a few patterns to recognize a lot of different microbes and endogenous ligands (such as fibronectin and hyaluronic acid)

Such as:highly conserved lipid A portion of lipopolysaccharide, or direct CD14-recognizing and -binding lipopolysaccharide or toll-like receptor 4 (TLR4) which recognize about 10 patterns and then activates proinflammatory transcription factors (NFkB) or MHCII on macrophages

Front 305

Describe how changes in the VA/Q ratio contribute to hypoxemia and shunt.

Back 305

areas of high VA/Q ratio cause inefficient ventilation (VA/Q &#56319; is infinity is dead space

and areas of low VA/Q ratio cause hypoxemia (VA/Q &#56319;0 is is 0 is a shunt) because of perfusion of poorly or nonventilated alveoli

In ARDS, gas exchange is affected by increases in the dispersion of both alveolar ventilation and cardiac output because bronchial and vascular functions are altered by disease-related factors, such as the effects of inflammatory mediators on airway and vascular smooth-muscle tone. Beause CO2 exchange is determined by alveolar ventilation reas of high VA/Q ratio and dead space in ARDS increase the ventilation required to keep the arterial PCO2 level constant. As lung compliance decreases, the work to expand the lungs to maintain the arterial PCO2 level must alsothe lungs to maintain the arterial PCO2 level must also increase. Hypoxemia produced by alveolar edema is most important to gas exchange in the acute phase. Pulmonary edema causes hypoxemia by creating areas of low VA/Q ratio and shunt; the latter cannot be overcome by oxygen administration because of the absence of alveolar ventilation

Front 306

Identify two physiologic parameters that regulate fluid exchange between capillaries and interstitial spaces and 3 aspects of “safety factor” that prevent pulmonary edema.

Back 306

Capillary fluid filtration is determined by the hydrostatic and osmotic pressure gradients across the capillary wall, as described by the Starling equation: simplified net (hydrostatic) filtration pressure- net osmotic (oncotic) pressure

Safety Factor- change in absorption forces caused by increased filtration pressure, capacity of the interstitial space to absorb fluid, and capacity of the lung’s lymphatic system to transport fluid out of the lung. These mechanisms maintain dry alveoli even when microvascular capllary pressure is moderately elevated, such as during exercise, hypoxia, or with compensated mitral stenosis.

Normal is 21 mm Hg for the healthy lung

Front 307

Explain how “safety factor” is compromised to make protein-rich edema in alveoli.

Back 307

As capillary pressure increases, the edema factor is introduced
First, filtration pressure increases and diluted fluid from the capillaries enters the interstitial space. The dilution decreases interstitial osmotic pressure, which increases the absorption force opposing the hydrostatic pressure. Second, as the interstitial pressure increases, interstitial fluid enters the perivascular space where lymphatic channels arise. The perivascular space swells, causing perivascular cuffing and interstitial edema without affecting gas exchange. The third component of the safety factor is the actual removal of interstitial fluid by the lymphatic system, which has at least an order of magnitude of reserve flow capacity

The interstitial fluid pressure exceeds the safety factor when interstitial volume increases by about 40%, and alveolar flooding will begin. The barrier collapses suddenly and plasma proteins of all sizes pass through.

Protein rich edema impairs gas exchange by excluding oxygen and inactivating surfactant,

Front 308

Describe the pathophysiologic consequences of alveolar flooding in ARDS.

Back 308

Protein rich edema impairs gas exchange by excluding oxygen and inactivating surfactant

In ARDS, permeability edema occurs because capillary conductance increases( this regulates the lymphatic flow) and the reflection coefficient decreases (the interstitial osmotic pressure becomes higher around leaky capillaries. This shifts the pressure–fluid curve of the lung to the left because the net absorption force in the Starling equation is minimized by capillary leakiness.

ARDS, the edema safety the edema safety factor decreases by about half, and flooding develops at lower capillary pressures. Pulmonary edema may actually contribute to the pathogenesis of ARDS

Front 309

Explain the roles of endothelial activation and epithelial damage in ARDS, and the mechanisms involved in epithelial repair.

Back 309

that pulmonary endothelial cells are activated in ARDS because pulmonary vascular endothelial integrity is often preserved microscopically even at sites of leukocyte accumulation

Endothelial activation-new protein was synthesized in response to endothelial cell activation. endothelial cell activation participates and partly drives the neutrophil inflammatory response that contributes to edema formation and fibrosis- also expression of adhesion and signaling molecules, which facilitate leukocyte adherence, coagulation is activated, tissue factor is produced, and fibrinolysis is inhibited; the resulting procoagulant environment and therefore pro-inflammatory

After an acute lung injury, the alveolar epithelium seems to resist more injury than the adjacent endothelium. Repair requires II alveolar epithelial cells, which are progenitors of the type I and type II. Type II cells are more robust than type I cells,

Optimal repair requires an intact basement membrane and provisional fibrin matrix to provide a platform for cell adhesion, spreading, and migration.

Front 310

Describe two physiologic benefits and two potential risks of using PEEP.

Back 310

Positive end-expiratory pressure improves oxygenation in ARDS by stabilizing damaged alveoli and improving areas of low VA/Q ratio and shunt . PEEP may also prevent further injury from repeatedly opening and closing alveoli. However, risks include oxygen toxicity, lung overdistention, and destructive cycles of alveolar opening and closure. increasing in lung water, lung stretch

Front 311

Identify two goals of using lung-protective mechanical ventilation to treat ARDS.

Back 311

, ventilation with lower tidal volumes and lower peak airway pressures (

Front 312

Identify two major mechanisms that serve to classify causes of pulmonary edema.

Back 312

1. HEMODYNAMIC EDEMA

2. EDEMA DUE TO MICROVASCULAR INJURY (ALVEOLAR INJURY)

Front 313

Name 3 causes of increased hydrostatic pressure, 3 disorders causing
hypoalbuminemia, and 7 causes of microvascular injury.

Back 313

Increased hydrostatic pressure (increased pulmonary venous pressure)
1. Left-sided heart failure
2.Volume overload
3. Pulmonary vein obstruction

decreased oncotic pressure
1. Hypoalbuminemia
2. Nephrotic syndrome
3. Liver disease
4. Protein-losing enteropathies

EDEMA DUE TO MICROVASCULAR INJURY (ALVEOLAR INJURY)
Infections: pneumonia, septicemia, Inhaled gases: oxygen, smoke, Liquid aspiration: gastric contents, near-drowning, Drugs and chemicals: chemotherapeutic agents (bleomycin), other medications (amphotericin B), heroin, kerosene, paraquat
Shock, trauma, Radiation
Transfusion

Front 314

Compare histologic features of exudative vs. proliferative vs. fibrotic stages of
diffuse alveolar damage

Back 314

In the acute stage, the lungs are heavy, firm, red, and boggy, havecongestion, interstitial and intra-alveolar edema, inflammation, fibrin deposition, and diffuse alveolar damage. alveolar walls become lined with waxy hyaline membranes like hyaline membrane disease of neonates. Alveolar hyaline membranes consist of fibrin-rich edema fluid mixed with the cytoplasmic and lipid remnants of necrotic epithelial cells. In the organizing stage, type II pneumocytes undergo proliferation, and there is a granulation tissue response in the alveolar walls and in the alveolar spaces. In most cases the granulation tissue resolves, leaving minimal functional impairment. Sometimes, however, fibrotic thickening of the alveolar septa ensues, caused by proliferation of interstitial cells and deposition of collagen. Fatal cases have superimposed bronchopneumonia.

Front 315

Describe how nuclear factor-κβ, IL-8, neutrophils, and dysregulated coagulation

Back 315

Although the cellular and molecular basis of acute lung injury and ARDS remains an area of active investigation, it appears that in ARDS, lung injury is caused by an imbalance of pro-inflammatory and anti-inflammatory mediators.[4] The most proximate signals leading to uncontrolled activation of the acute inflammatory response are not yet understood. However, nuclear factor κB (NF-κB), a transcription factor whose activation itself is tightly regulated under normal conditions, has emerged as a likely candidate shifting the balance in favor of a pro-inflammatory state. As early as 30 minutes after an acute insult, there is increased synthesis of interleukin-8 (IL-8), a potent neutrophil chemotactic and activating agent, by pulmonary macrophages. Release of this and similar compounds, such as IL-1 and tumor necrosis factor (TNF), leads to endothelial activation, and pulmonary microvascular sequestration and activation of neutrophils. Neutrophils are thought to have an important role in the pathogenesis of ARDS

Front 316

. Identify two conditions responsible for most deaths in patients with ALI/ARDS.

Back 316

The majority of deaths are attributable to sepsis or multi-organ failure and, in some cases, direct lung injury.[6]

Front 317

Describe how three cell types contribute to resolution of diffuse alveolar damage.

Back 317

Pro-inflammatory cytokines such as interleukin 8 (IL-8), interleukin 1 (IL-1), and tumor necrosis factor (TNF) (released by macrophages), cause neutrophils to adhere to pulmonary capillaries and extravasate into the alveolar space, where they undergo activation. Activated neutrophils release leukotrienes, oxidants, proteases, and platelet-activating factor (PAF), which contribute to local tissue damage, accumulation of edema fluid in the airspaces, surfactant inactivation, and hyaline membrane formation. Macrophage migration inhibitory factor (MIF) released into the local milieu sustains the ongoing pro-inflammatory response. Subsequently, the release of macrophage-derived fibrogenic cytokines such as transforming growth factor β (TGF-β) and platelet-derived growth factor (PDGF) stimulate fibroblast growth and collagen deposition associated with the healing phase of injury

Front 318

Compare definitions of diffuse alveolar damage/ALI vs. acute interstitial pneumonia

Back 318

Acute interstitial pneumonia is a clinicopathologic term that is used to describe widespread ALI associated with a rapidly progressive clinical course that is of unknownetiology (sometimes referred to as idiopathic ALI-DAD

Front 319

Identify two permanent pathophysiologic sequelae of DAD in the fibrotic stage.

Back 319

death or chronic interstitial disease may develop

Front 320

Markus: Vascular Disorder

Define pulmonary HTN

Back 320

Sustained mean pulmonary artery pressure exceeds 25 mmHg at rest or 30 mmHg with exercise

Front 321

what is the normal pulmonary pressure

Back 321

15mm Hg

Front 322

why can Sickle cell anemia be a trigger for elevated pulmonary arterial pressure

Back 322

free hemoglobin scavenges nitric oxide, endothelin rises, and vessels constrict

Front 323

define Cor pulmonale

Back 323

right heart failure due to pulmonary HTN

Front 324

what are the early vs late effects of pulmonary HTN

Back 324

Transient or early hypoxemia or volume overload causes transient pulmonary hypertension; in hypoxemia through reflexive vasoconstriction. This process is reversible.

After repetitive triggers however, there is intimal and medial wall thickening and eventually fibrosis with a permanent elevation in pulmonary pressures.

Front 325

name 5 findings on physical exam of a pt with pulmonary HTN

Back 325

Increased intensity of the pulmonic component of the second heart sound
Diastolic murmur of pulmonary regurgitation
Left parasternal lift
Jugular venous distension
Hepatomegaly, ascites, peripheral edema

Front 326

Idiopathic (sporadic) PH carries a poor prognosis, what medications should patients be put on for life

Back 326

All should receive lifelong anticoagulation due to high incidence of pulmonary thrombosis and thromboembolism due to stasis of blood and sedentary lifestyle

Front 327

List 3 FDA approved treatments for idiopahtic PH

Back 327

Calcium channel blockers,

prostacyclin analogues,

endothelin-receptor antagonists

Front 328

list the risk factors for developing a Pulmonary embolism

Back 328

Immobilization
CHF
Surgery within last three months
History of previous thromboembolism
Malignancy
Pregnancy
Lifestyle factors- smoking
Medications (estrogen, progesterone, raloxifene)
Hypercoagulable state (ProteinC, S, or antithrombin II deficiency, Lupus)

Front 329

what are the classic presentations of pt with a major Saddle embolus?

Back 329

With inability to empty the RV, there is decreased cardiac output and systemic hypotension.

classic impending dome

Front 330

what is the classic finding on an EKG of a pt with pulmonary embolism

Back 330

This is the typical right heart strain pattern – S1, Q3, T3.

Front 331

what would the blood gases be of this pt

Back 331

With embolism there may be reduced arterial pO2 and usually reduced pCO2 as well.

Front 332

what is the D-dimer level in this pt

Back 332

D-dimer- degredation product of cross-linked fibrin. Indicates fresh clot. If high, somewhat non-specific (especially post-op). If LOW, pulmonary embolus or DVT very UNLIKELY

Front 333

how can this CXR help you differentiate between PE and Infacrction

Back 333

Embolism
Normal
Decreased vascular markings
Elevated hemi-diaphragm

Infarction
Wedge-shaped densities
Pleural based density
“Hampton’s hump”
Pleural effusion

Front 334

describe the presentation of a pt with Alveolar Hemorrhage

Back 334

Pink frothy sputum
Blood-tinged sputum
Frank hemoptysis
Common causes include CHF and acute bronchitis or pneumonia

Front 335

list 3 causes of alveolar hemorhage

Back 335

Systemic vasculitis – Wegener’s

Collagen vascular disease - SLE

Goodpastures’s

Front 336

Cystic Fibrosis lecture

t/f CF is AD

Back 336

false- AR

Front 337

describe the CF gene defect

Back 337

The gene affected in CF encodes for the protein cystic fibrosis transmembrane conductance regulator (CFTR). CFTR facilitates the chloride transport of electrolytes across cell membranes in the epithelial lining of the ducts of exocrine glands, including sweat and mucus-producing glands. long (q) arm of chromosome 7. The most common mutation in caucasians (approx. 70%) is a deletion of phenylalanine at base pair 508 on the CFTR gene.

Front 338

Describe a Class I - Defective protein production of CFTR

Back 338

Class I - Defective protein production — This defect is usually caused by nonsense, frameshift, or splice-site mutations, leading to premature termination of the mRNA and complete absence of CFTR protein.

Front 339

Describe a Class II - Defective protein processing of CFTR

Back 339

Class II - Defective protein processing — With class II defects, the mutations in the CFTR sequence prevent the protein from trafficking to the correct cellular location. The most common CFTR mutation, delta F508 (deletion of a single phenylalanine residue in the first NBF), belongs to this category.

Front 340

describe a Class III - Defective regulation in CFTR

Back 340

Class III - Defective regulation — These mutations lead to diminished channel activity in response to ATP. Many involve alterations of the NBF regions, NBO1 and NBO2, which may retain varying degrees of sensitivity to nucleotide binding.

Front 341

how does a dysfunctional CFTR protein increase the risk of infections in pt with CF

Back 341

defective cellular transport of chloride and sodium across epithelial cell membranes. Sweat becomes abnormally salty and mucus in the respiratory tract, GI tract, or reproductive tract is abnormally viscous. Mutant CFTR aggravates the development of pulmonary infection by promoting initial bacterial adhesion by upregulating epithelial cell adhesion molecules for bacteria and by decreasing the production of innate host defense molecules, such as nitric oxide.

Front 342

what types of infections are pt with CF more likely to have

Back 342

H. influenza
Staph aureus
MRSA
Pseudomonas aeruginosa
Burkholderia cepaciae
Aspergillus fumigatus

Front 343

what is the pathogenesis of this CF pts symtoms

Back 343

brochioectasis- Bronchial mucous plugging causes partial and complete blockages of airways. The lung develops areas of atalectasis and other areas of air trapping. Blockages also facilitate inflammation. Pathogens (bacteria and fungi) may become trapped and colonize the airways. Smoldering infection aggravates inflammation. Eventually, bronchi become bronchiectatic: they become dilated and lose adequate cartilaginous supports. Bronchiectasis further impairs mucous clearance from the respiratory tract

Front 344

what are the 3 physicial signs associated with this CF pts condition

Back 344

Bronchiectasis is associated with productive cough, clubbing, and the development of “barrel chest”.

Front 345

what would be an indication that a newborn has CF

Back 345

Meconium ileus occurs when the meconium is abnormally thick and obstructs the GI tract.

Front 346

what is meconium

Back 346

Meconium is the 1st bowel movement that a newborn passes. It consists of bile salts, bile acids and debris shed from the intestinal epithelial lining during embryonic life.

Front 347

describe the systemic effects and complications of CF

Back 347

Unlike endocrine glands (which release secretions into the bloodstream), exocrine glands release secretions through ducts. The highest concentrations of CFTR are in the submucosal exocrine glands in the airways, pancreas, salivary glands, sweat glands, intestines, and reproductive tract

Front 348

in newborn screening, what test is done to look for CF

Back 348

Immunoreactive trypsinogen (IRT) from heel blood spot

Elevated IRT leads to 2nd tier of testing
Positive screen (IRT and 2nd tier) then sweat test

Front 349

describe the pancreatic problems in pt with CF

Back 349

thick secretions produced within the pancreas partially or completely block the ducts leading to the small bowel. Duct obstruction prevents pancreatic enzymes from entering the intestine. The result is incomplete digestions of fats and proteins as well as poor absorption of fat soluble nutrients (vitamins).

Front 350

what conditions are associated with pancreatic insufficiency in pts with CF

Back 350

Failure to thrive
Steatorrhea
Weight loss fat soluable vitamin deficiency
Abdominal pain
Bloating, distension, excessive flatus
Meconium ileus
Distal intestinal obstruction syndrome
Rectal prolapse

Front 351

describe the unique lesions of the liver in pt with CF

Back 351

Focal biliary cirrhosis is characterized by concretions of eosinophilic material plugging the bile ductules, biliary proliferation, inflammatory reaction, and absence of marked bile stasis in the surrounding liver parenchyma.

Front 352

what is The most common long term antibiotic therapy for pt with CF

Back 352

The most common long term antibiotic therapy are inhaled antibiotics (tobramycin is most common, though others are near the market, such as aztreonam)

Front 353

which The mucus thinning agents are used in pts with CF

Back 353

The mucus thinning agents used are DNAse (Pulmozyme) and inhaled 7% saline (which hydrates CF mucus and promotes cough).

Front 354

what immunizations are given to pt with CF

Back 354

Immunizations mean influenza and pneumoccocus, predominately. Palimizumab (a passive immunization against RSV virus) is often provided to CF infants.

Front 355

Which drugs are used for the common bacterial infections in pt with CF

Back 355

Front 356

what are the signs and symptoms of respiratory distress in newborns

Back 356

tachypnea, grunting, flaring, retractions, hypoxemia, cyanosis

Front 357

what is the difference between newborn respiratory distress and respiratory distress syndrome

Back 357

Respiratory Distress Syndrome in Newborns
Term generally reserved for respiratory distress associated with prematurity, and surfactant deficiency or surfactant abnormalities.

Front 358

how does a newborn present with respiratory distress syndrome

Back 358

Acute illness characterized by increased RR, grunting, retractions, dyspnea that develop in the first hours after birth.

Front 359

what are the risk factors for hyaline membrane disease

Back 359

IRDS-
Pre-term labor
Premature rupture of amniotic membrane
Placental insufficiency
Chorioamnionitis
Cesearan section delivery
Infant of diabetic mother

Front 360

what is the treatment of an newborn with IRDS

Back 360

Exogenous surfactant
Antenatal corticosteroid administration
Supplemental Oxygen
Mechanical ventilation
CPAP, Positive pressure controlled ventilation
Diuretics

Front 361

what is Bronchopulmonary Dysplasia

Back 361

A chronic lung disease of infancy associated mostly with prematurity.
BPD appears to be the final common pathway of lung injury.
Premature lungs + O2 toxicity + ventilator baro-trauma + inflammatory response leads to BPD.

Front 362

Describe the pathology of this infant that died of Bronchopulmonary Dysplasia

Back 362

BPD is disruption of lung development. Decreased septation and alveolar hypoplasia lead to fewer and larger alveoli. Reduced microvascular development also may occur.

Front 363

describe the pathophysiology that leads to bronchopulomonary dysplasia

Back 363

BPD is associated with increased airway resistance, decreased lung compliance, increased airway reactivity, and increased airway obstruction.

injury to the pulmonary circulation can lead to pulmonary hypertension and cor pulmonale, which substantially contribute to the morbidity and mortality associated with severe BPD.

Front 364

what is the treatment for BPD

Back 364

Support good growth
Support ventilation and oxygenation
Bronchodilators
Diuretics
Systemic corticosteroid

Front 365

describe the FRC in a pt with IRDS or BPD

Back 365

.His functional residual capacity (FRC) is low at 56% predicted (which is expected in RDS and advanced BPD).

Front 366

an infant with brochopulmonary dysplasia will have a curve that looks more like (emphysema or fibrosis) Why

Back 366

the fibrotic lung is stiff with low compliance and the emphysematous lung is more complaint.

In emphysema, lung compliance decreases with increasing volume. Therefore as the lung increases in size, more pressure must be applied to get the same increase in volume.

Front 367

Describe the Lung interstitium

Back 367

encompasses the space between alveolar epithelium and capillary endothelium. It includes the blood vessels, connective tissues surrounding the blood vessels, lymphatics and terminal airways.

Front 368

list 7 Systemic Rheumatoid Disorders associated with interstitial lung disease

Back 368

RA, SLE, scleroderma, ankylosing spondylitis, mixed connective tissue disease, polymyositis/dermatomyositis, Sjogrens

Front 369

list 6 environment-occupations associated ILD

Back 369

Organic-Hypersensitivity pneumonitis, Famer's lung

Inorganic- Silicosis, Asbestosis, Beryliosis, Coal Worker's pneumonicosis

Front 370

which alveolar filling disorder is associated with ILD

Back 370

Goodpasture's

Front 371

IDL is associated with which two vasculitis disorders

Back 371

Wegner's and Churg-Strauss

Front 372

ILD is associated with which 5 inherited disorders

Back 372

Familial idopathic pulmonary fibrosis, Neimann-Pick, Gaucher, Neurofibromatosis, Tuberous Sclerosis

Front 373

DDx

Tachypnea, Crackles at both lung bases, Signs of right sided heart failure , Hilar or mediastinal adenopathy

Back 373

Sarcoidosis

Silicosis (egg shell calcification)
Lymphocytic interstitial pneumonia
Amyloidosis

Gaucher’s disease

Front 374

DDx:

Tachypnea, Crackles at both lung bases, Signs of right sided heart failure , Upper lobe involvement

Back 374

Ankylosing spondylitis

Berylliosis

Histiocytosis X

Silicosis

Chronic hypersensitivity pneumonitis

Front 375

In addition to Tachypnea, Crackles at both lung bases, Signs of right sided heart failure . What is highly suggested sign of Idiopathic Pulmonary Fibrosis(Cryptogenic Fibrosing Alveolitis)

Back 375

clubbing

Dyspnea insidious in onset, at least for 2-3 years

Front 376

what is Caplans’s Syndrome

Back 376

Described in coal workers with rheumatoid arthritis.
Presence of rounded densities in these patients which undergo cavitation.

Front 377

why would ACE levels be elevated in a pt with Sarcoidosis? In what other conditions is ACE elevated?

Back 377

ACE-converts angiotensin I to angiotensin II, usually produced by capillary endothelial cells, also produced by alveolar macrophages.

elevated in 60% of patients with active dis.

Also elevated in cases of silicosis, asbestos exposure, Gauchers dis, leprosy, coccidiodomycosis, miliary TB, IBD

Front 378

In a pt with Silicosis, describe the pt population and CXR,

Back 378

Silicosis-Inhalation of free crystalline silica dust

Foundry worker, sandblaster, tunneling, pottery making

Cxray with upper lobe nodules with egg shell calcifications of hilar nodes.

Front 379

t/f pt with silicosis are at high risk for Tb

Back 379

true- Patients at high risk for typical as well as atypical Mycobacterial infections

Front 380

what occupations expose a person to asbestos

Back 380

Shipyard workers, pipefitters, welders, sheet metal workers, workers involved in automotive repair esp. brake lining work.

Front 381

Coal Worker Pneumoconiosis is associated with inhalation of coal, where are the nodules usually located on CXR

Back 381

Simple CWP: nodules which are less then 1 cm in size with predilection for upper lobes.

Complicated CWP: presence of density of more then 1cm in size

Front 382

what is the most common fungi affecting people with Hypersensitivity Pneumonitis?

what is hypersensitivity pneumonitis

Back 382

Actinomycetes

Secondary to inhalation of organic dust derived from animal dander and proteins or saprophytic fungi contaminating water reservoir, dairy products, wood bark and animal droppings.

Front 383

why is Chronic eosinophilic pneumonias confused with Tb? what is the treatment

Back 383

Usually presents with chronic sxs of cough, night sweats and wt. Loss

Cxray shows infiltrates in lung periphery

Blood eosinophilia is absent

Treatment is steroids

Front 384

in general, what is the Ddx for an ear infection, and treatment

Back 384

ear- viral, strep pneumo, antihistamines and decongestants

Front 385

in general, what is the Ddx for an nose infection, and treatment

Back 385

nose-bacterial- H. flu, antibiotics

Front 386

in general, what is the Ddx for an throat infection, and treatment

Back 386

throat-allergic- M. catarrhalis, steroids, nasal spray

Front 387

how will this pt present?

which pathogens are associatd and what drugs are used?

Back 387

with itching or pain in the ear canal, Sometimes discharge
Usually painful to touch the ear lobe or lie on that ear at night

Topical drops directed at usual pathogens: Strep, Staph, fungus, Pseudomonas
Possibly use wick

Front 388

how will this pt present?

which pathogens are associatd and what drugs are used?

Back 388

Swimmers ear- with itching or pain in the ear canal, Sometimes discharge
Usually painful to touch the ear lobe or lie on that ear at night

Topical drops directed at usual pathogens: Strep, Staph, fungus, Pseudomonas
Possibly use wick

Front 389

what 3 signs or symptoms must the pt have?

what are the usual pathogens?

what are the usual treatments?

Back 389

acute otitis media- Acute 1.onset of signs and symptoms
2.Presence of middle ear effusion: bulging,
decreased movement of TM, air/fluid levels
3.Middle ear inflammation: redness of TM or otalgia

Strep. Pneumoniae, Hemophilus Influenza, and Moraxella Catarrhalis and pain control. Usual treatment is with antibiotics for 10 days.

Front 390

what symptoms are associated with this condition?

Back 390

AOM-Fever, ear pain (is not worsened by moving the earlobe), decreased hearing, vertigo

Current or recent setting of “a cold”

In babies, sometimes pulling at ears or irritability: won’t drink or lie down

Front 391

what is the drug of choice for this condition? what is an option for those that don't respond to the typical treatment early on?

Back 391

Amoxicillin at a dose of 80-90 mg/kg given twice a day is the drug of choice followed by

Augmentin for early non-responders(Amoxicillin/clavulanate )

Front 392

this Characteristic bluish tint to the inferior turbinate is classic in which condition?

What is the treatment

Back 392

allergic rhinitis

The mainstays of treatment are anti-histamines [Antihistamines:
Loratadine (Claritin)
Cetirizine (Zyrtec) ] and nasal steroid sprays-Flonase, Nasacort

Front 393

The common cold, viral rhinitis, is associated with which 3 symptoms and what medication are prescribed?

Back 393

Abrupt onset with fever, chills or body aches

Gets better in 7-14 days w/o treatment

Can suggest- Decongestants and fever relievers.The best decongestant is pseudoephedrine HCL (Sudafed)

Front 394

what are the signs and symptmos of sinusitis?

which organisms are usually at fault.

how is this different from viral rhinitis?

name 4 finding on physical exam

what is the treatment

Back 394

1. Headache: facial, frontal, or between eyes , Congestion
Sometimes fever,

2. S. pneumoniae, H. flu, M. catarrhalis

3. No rhinorrhea

4. red turbinates with pus emanating, May see PND in throat, Swelling/Tenderness to palpation of sinuses
Transillumination:opacification

5.Antibiotics: Amoxicillin, TMP/SMX for 7-14 days, Recurrent sinusitis: consider anaerobes Clindamycin

Front 395

what is the treatment

Back 395

Topical anti-fungal: nystatin “Swish and Swallow”, Mycostatin troches, Diflucan pills

Rinse mouth after inhaled steroid MDI use

Front 396

what is the treatment

Back 396

Fever Blisters”
Treat with acyclovir, famciclovir, valacyclovir pills

Front 397

t/f Pharyngitis (Sore Throat)Etiology is usually bacterial

Back 397

false- usually viral

Rhinoviruses, Adenoviruses, Influenza A+B, Respiratory Syncytial Virus (RSV), Parainfluenza
Also seen with Epstein-Barr, CMV, Measles

Front 398

Streptococcal Pharyngitis

how will this patient present

what is the treatment

Back 398

Prominent dysphagia, fever, “Hot potato” voice, huge Tonsils & exudate,Petechiae on palate, no cough or No cough/rhinorrhea, HA or stomach ache


Penicillin is drug of choice
Erythromycin for PCN allergic pts

Front 399

croup-

list the 3 classic findings

what is treatment

Back 399

Laryngotracheitis is the inflammation of the larynx and trachea.

classic triad of inspiratory stridor, a harsh barking cough, and hoarseness

Since it is a viral illness, if there is no respiratory distress, simply waiting it out is enough treatment or cool mist vaporizers , Severe cases may need evaluation for respiratory distress and treatment for wheezing and edema of airway, Oral steroids

Front 400

Epiglottis

what are the physical exam findings?

which pathogens are usually associated?

what is treatment

Back 400

Anxious appearance, Prominent drooling, Child prefers sitting up, leaning forward, chin hyper-extended
Inspiratory stridor, retractions, fatigue and cyanosis are late findings

Caused by H. flu or strep

Treat with IV cephalosporins
Treat household and daycare contacts with oral Rifampin

Front 401

t/f Humans and animals are the only known reservoir for tuberculosis

Back 401

false -only humans

Front 402

how is Tb transmitter

Back 402

Transmission - airborne droplet nuclei

Front 403

what are the symptoms of Tb

Back 403

Productive cough
Fever and night sweats
Weight loss
Hemoptysis (late symptom)
Chest pain
Anorexia
Fatigue

Front 404

t/f lower lobe involvement is most common in Tb

Back 404

false- Upper lobe involvement is most common

Front 405

what is Miliary TB

Back 405

numerous small nodular lesions (resembling millet seeds)

Front 406

Decribe the what a Ghon complex is and how it is formed as shown on CXR

Back 406

The Ghon's complex is a combination of the Ghon's focus (arrow, area of initial infection in the lung) and a lymphatic lesion. Approximately two to three weeks after the Ghon's focus has developed, the area undergoes necrosis. Free bacilli, or bacilli within macrophages, drain from the area into the affected lungs' lymph nodes. Typically these areas heal with calcification visible on chest X-ray.

Front 407

Describe the organism in the picture, the stain used and if what are the tuberculin skin test 5mm diameter cut offs,

Back 407

Positive Acid-Fast B smear, numerous red organisms present.

1.Close contacts to persons with newly diagnosed tuberculosis
2) HIV positive
3) Organ transplant
4) Corticosteroids (>15 mg per day prednisone or equivalent for > 1 month)
5) Patients with fibrotic lesions on chest x-ray (not granulomas)

Front 408

what are the 10mm cut offs for this disease

Back 408

Recent converter - at least 10 mm increase in skin test in past 2 years
-Weight loss > 10% of ideal body weight
-Children < 4 years old
-Residents and employees from health care, homeless, or long-term care facilities
-Recent immigrant (past 5 years) from a high-prevalence country

Front 409

what are the 10mm cut offs for this disease

Back 409

Recent converter - at least 10 mm increase in skin test in past 2 years
-Weight loss > 10% of ideal body weight
-Children < 4 years old
-Residents and employees from health care, homeless, or long-term care facilities
-Recent immigrant (past 5 years) from a high-prevalence country

Front 410

what is the TST cut off for 15mm

Back 410

No risk factors for TB
Not always treated
Usually seen in an individual being hired to a position in high risk setting

Front 411

what are the complications that could be associated with Tb. What is noted on this pt

Back 411

Aspergilloma: “crescent sign” on this CXR
Hemoptysis
Broncholithiasis
Fibrothorax
Carcinoma (controversial)

Front 412

if a pregnant pt present with this stain. Which of the first line drugs will not be used and why

Back 412

streptomycin, bc aminoglycosides are teratogenic

Front 413

which drugs are used for a Mycobacterium avium Complex and for how long

Back 413

Primary drugs
Rifabutin
Azithromycin
Quinolones
Ethambutol
Streptomycin

Therapy requires 3 or more drugs for 12-18 months

Front 414

what is this organism and what is its route of dissemination once inside the body

Back 414

Histoplasmosis

Hematogenous dissemination occurs

occurs in Ohio River valley

Front 415

name the organism and what will CXR show. Describe physical exam

Back 415

Chest x-ray: hilar/mediastinal lymph nodes, patchy infiltrates
Rheumatologic manifestations
Erythema nodosum-tender, red nodules under the skin most common
on the shins

Front 416

name the organism inside this cell and how is the diagnosis made

Back 416

histoplasmosis inside macrophage

Antigen Tests
Urine positive in 90 % of patients with disseminated disease
Sensitivity lower in serum than urine, the highest yield achieved by testing both

Front 417

what is the treatment for this organism

Back 417

histoplasmosis- Antifungal choices
Amphotericin B
Itraconazole

Corticosteroids
Acute infection with severe hypoxia
Granulomatous mediastinitis

Front 418

in what areas is this organism located

Back 418

histoplasmosis in ohio river valley

Front 419

what kind of conditions can this organism cause if left untreated

Back 419

, chronic skin ulcer due to Blastomycosis

Front 420

where is this organism found

Back 420

Blastomyces dermatitidis, a dimorphic fungus.

Blastomyces is endemic to the Mississippi and Ohio river valleys and the vicinity of the Great Lakes.

Front 421

what is this organism and in what area is it located

Back 421

Coccidioidomycosis-also known as "California disease, "Desert rheumatism,"San Joaquin valley fever," and "Valley fever"

Arizona, California, Nevada, New Mexico, Texas, Utah and northwestern Mexico.[3]

Front 422

in what pt population is this more likely.

what symptoms will the pt experience

how will this look on CXR

what it the treatment

Back 422

Pre-existing pulmonary cavities (COPD, prior TB)

Minimally invasive

Hemoptysis: invasion of blood vessels

Asymptomatic crescent-nodule on chest x-ray

CT: rim of air around mass
Tx: resection, itraconazole

Front 423

t/f humans are the only reservoir

Back 423

true- bordetella pertussis- whooping cough

Front 424

describe the Catarrhal phase of bordetella pertussis

Back 424

. Rhinorrhea, lacrimation, low-grade fever, sneezing, and mild cough are characteristic. Patients can develop a leukocytosis > 50,000 cells/mm3, with a relative lymphocytosis.

Front 425

describe the Paroxysmal phase of bordetella pertussis

Back 425

Lasts 1-6 weeks
Paroxyms of coughing (up to 30/day)
Coughing followed by “whoop” or gasp
Post-tussive emesis
Cough may be productive

Front 426

describe the Convalescent phase of bordetella pertussis

Back 426

Lasts 2-3 weeks
Paroxysms are less common
Coughing decreases

Front 427

what is the gold standard for testing for this organisms

Back 427

Culture from nasopharynx is the gold standard for pertussis

Front 428

what is the drug of choice and duration for this organism

Back 428

. Erythromycin is the antibiotic of choice, standard treatment course is 14 days. for bordetella pertussis

Front 429

Markus- Pneumonia

"Pneumonia" is a term used to indicate inflammation of the which part of the lung:

Back 429

e inflammation of the distal lung:
1. terminal airways,
2. alveolar sacs and
3. interstitium.

Front 430

list the 4 routes that Infectious agents gain entry to the lower respiratory tract through

Back 430

1. microaspiration of oropharyngeal secretions: pneumococcus, anaerobes

2. inhalation of airborne material: TB, Legionella, viral

3. metastatic seeding of the lung from blood: S. aureus

4. direct extension: amoebic liver abscess

Front 431

describe the Pathophysiology of Pneumonia

Back 431

The invading organism causes symptoms, in part, by provoking an inflammatory
response in the lungs

The capillaries become leaky, and protein-rich fluid seeps into the alveoli.

This results in a less functional area for oxygen-carbon dioxide exchange.

Front 432

describe the result of Mucus plugs decrease the efficiency of gas exchange in the lung during pneumonia

Back 432

The alveoli fill further with fluid and debris from the large number of white blood
cells being produced to fight the infection.

The patient becomes relatively oxygen deprived, while retaining carbon dioxide.
The patient breathes faster and faster, in an effort to bring in more oxygen and blow off more carbon dioxide.

Front 433

describe Consolidation in pneumonia

Back 433

Consolidation, a feature of bacterial pneumonias, occurs when the alveoli, become
solid, due to quantities of fluid and debris.

Red (early) hepatization
Grey (late) hepatization

Front 434

what is the most important causes of death in patients with acute pneumococcal pneumonia

Back 434

Respiratory Failure

but pneumonia also causes:
Ventilatory failure
Hypoxemic respiratory failure

Front 435

what causes the Ventilatory Failure in pneumonia

Back 435

Caused by mechanical changes in the lungs resulting from pneumonia.Inflammatory exudate fills alveoli at slightly less than their normal functional residual
capacity (FRC)

Resulting volume loss at FRC roughly proportional to the extent of the pulmonary
infiltrate.

Consolidated air space does not inflate easily at higher transpulmonary pressures so there is a Loss of volume:
1. reduces total lung compliance
2. increases the work of breathing.

Front 436

what causes the Hypoxemic Respiratory Failure in pneumonia. what is the effect of the result of hypoxemic respiratory failure

Back 436

Arterial Hypoxemia early in acute pneumococcal pneumonia due to:
Persistence of pulmonary artery blood flow to consolidated lung
Resulting in an intrapulmonary shunt

Front 437

t/f the Nasopharynx defense against pathogens includes:
Nasal hair, turbinates, IgG secretion, and Mucociliary apparatus

Back 437

false- IgA and
Nasal hair, turbinates,
Mucociliary apparatus

Front 438

is a CXR necessary for diagnosis of pneumonia?

Back 438

yes-CXR: ESSENTIAL for diagnosis

Front 439

when should a pt be considered to have Community Acquired Pneumonia (CAP)

Back 439

CAP should be considered when a patient presents with 2 or more of the following
symptoms: fever; chills; new-onset cough; change in sputum color or increase in the volume if there is a chronic cough; chest discomfort; or dyspnea.

Front 440

in which areas can pneumonia be caused by Hanta virus

Back 440

Hanta virus pneumonia occurs at higher rates in the “four corner area” in the US (CO, UT, NM, NE)

Front 441

t/f serum cultures are the most specific diagnostic test for the causative agent

Back 441

false- Blood cultures are the most specific diagnostic test for the causative agent

Front 442

Name the organism involved in this pneumonia:

Alcoholics
Lobar CXR
“currant Jelly” sputum
PMNs -Encapsulated gnr

Back 442

Klebsiella

Front 443

Name the organism involved in this pneumonia

Often elderly
Lobar CXR
“rusty” colored sputum
GP Diplococci “lancets”

Back 443

Streptococcus pneumonia

Front 444

Name the organism involved in this pneumonia

Younger
Interstitial CXR
Scant Pmn,
No organisms on gram stain

Back 444

mycoplasma pneumonia

Front 445

Name the organism involved in this pneumonia

COPD
Smoker
Lobar CXR
Purulent - (“safety pins”) bipolar staining

Back 445

H. influenza

Front 446

Name the organism involved in this pneumonia

Alcoholic,
Mental Status decreases
Multi- Lobar CXR
(Lower) Foul sputum
Mixed Organisms and Pmns

Back 446

Aspirate- of anaerobes

Front 447

Name the organism involved in this pneumonia

Prior Influenza
Lobar CXR Cavitary
Bloody sputum
Gpc in Clusters
Pmns

Back 447

staphylococcus pneumonia

Front 448

Definition:

represents an adaptation to the development of host
antibodies.

(antigenic drift or antigenic shift)

Back 448

antigenic drift

Front 449

Definition:

occurs as soon as a type A influenza virus with a completely novel hemagglutinin or
neuraminidase formation moves into humans from other host species.

Back 449

antigenic shift

Front 450

what is the function of Hemagglutinin in influenza

Back 450

Hemagglutinin derives its name from its activity. The virus the ability to agglutinate, red blood cells. functions in the binding of the virus to cells, via the recognition of sialic acid.

Front 451

what is the function of Neuraminidase in influenza

Back 451

Neuraminidase ( acetyl-neuraminyl hydrolase). The enzyme removes residues called N-Acetyl-neuraminic acid from chains of sugars and from other glycoproteins.
allows the virus to both pass out of the human epithelial cells in which it is replicating, and enter new cells to initiate a new round of viral replication.

Front 452

in diaganosing influenza, what is the gold standard

Back 452

Viral culture: “gold standard”

Front 453

Air Pollutants:

what are the 5 main air pollutants

Back 453

Carbon Monoxide (52 %)
Sulfur Dioxide (14 %)

Nitrogen Oxides (14 %)

Ozone (14 %)

Particulate matter (4 %)

Front 454

list 4 major sources of air pollutants

Back 454

1. Combustion of fossil fuels (motor vehicles)

2. Coal fired power plant emissions

3. Waste incinerators

4. Atmospheric reactions

Front 455

what are the major indoor pollutants

Back 455

Tobacco smoke
Gas and wood stoves
Furnaces
Construction materials
Furniture
Radon
Allergens

Front 456

list 2 Reducing type of pollution

Back 456

SO2 and smoke from incomplete combustion of coal)

Front 457

list 3 oxidizing type pollution

Back 457

Oxidizing or photochemical type (nitrogen oxides, hydrocarbons, and ozone