First Aid 2010: Respiratory

Front 1

What are Clara cells

Back 1

noncilliated, columnar w/secretory granules

secrete component of surfactant, degrade toxins, act as reserve cells

Front 2

Pneumocyte Type 1 ?

Back 2

97% of alveolar surfaces (line them), are squamous cells + optimal for gas diffusion

Front 3

What is indicative of fetal-lung maturity?

Back 3

lecithin:sphingomyelin ratio > 2.0

Front 4

Pneumocyte type II?

Back 4

cuboidal and clustered,

secrete surfactant, as a precursors to Type 1 cells and other Type 2 cells, proliferate during lung damage

Front 5

What is bronchopulmonary segment

Back 5

tertiary (segmental) bronchus and 2 arteries (bronchial and pulmonary)
(Arteries run w/Airways)

veins and lymphatics drain along borders

Front 6

What is the relationship of the pulmonary artery to the bronchus at each lung hilus?

Back 6

RALS

Right: Anterior
Left: superior

Front 7

What lung is a more common site for inhaled foreign body and why?

Back 7

Right lung, b/c the R main stem bronchus is wider and more vertical than the left

Front 8

What structures perforate the diaphragm at:
T8
T10
T12

Back 8

T8: IVC
T10: esophagus, vagus
T12: aorta, thoracic duct, azygous vein (red, white and blue)

Front 9

What muscles used for inspiration and expiration during quiet breathing?

during exercise?

Back 9

quiet/Normal: diaphragm (inspiration), passive (expiration)

exercise:
Inspiration: external intercostals, Scalene mm, Sternomastoids
Expiration: rectus abdominis, internal + external obliques, transversus abdominis, internal intercostals

Front 10

How do you calculate collapsing pressure?

During breathing, what increases the tendency for alveoli to collapse?

Back 10

P = 2T/r
T= tension, r=radius

Expiration --> smaller radius --> increased tendency to collapse

Front 11

What happens when there is a deficiency in surfactant in newborns?

Back 11

neonatal RDS or hyaline membrane disease

Front 12

What is vital capacity

Back 12

TV + IRV+ ERV

Front 13

What is functional residual capacity

Back 13

RV + ERV
volume in lungs after NL expiration

Front 14

What is inspiratory capacity

Back 14

IRV + TV

Front 15

How do you calculate physiologic dead space (Vd)?

Back 15

Vd = Vt + [(PaCO2 - PeCO2) / PaCO2]

Vt = tidal volume
PaCO2 = arterial PCO2
PeCO2 = expired air PCO2

Physiologic dead space = anatomic dead space + functional dead space (wasted ventilation e.g. apical lung due high V/Q)

Front 16

What part of the lung is the largest contributor of functional dead space?

Back 16

apex of healthy lungs

Front 17

What is physiological dead space

Back 17

anatomical dead space of conducting airways plus functional dead space in alveoli (volume of air that doesn't take part in gas exchange)

Front 18

When is inward pull of lungs balanced by outward pull of chest wall?

How does this change with emphysema? fibrosis?

Back 18

FRC (functional residucal capacity = RV + ERV)
when system pressure is atmospheric pressure

Emphysema: high compliance --> high FRC
Fibrosis: low compliance --> low FRC

Front 19

What are the 2 forms of adult hemoglobin

Back 19

T and R

T (taut) has low affinity for O2 (R shift)
R (relaxed) has high affinity for O2 (L shift)

Front 20

What conditions favor Right shift or T form of Hb?

Back 20

increases in:
Cl-, [H+]/altitude, CO2, 2,3-BPG, exercise/metabolic needs, temperature

lead to increase O2 unloading to tissue

Front 21

How is methemoglobin treated

Back 21

methylene blue

Front 22

How do you treat cyanide poisoning

Back 22

use nitrites to oxidize Hb to methemoglobin (Fe 3+ form), which binds cyanide (this allows cytochrome oxidase to resume function),
then use thiosulfate to bind cyanide -> thiocyanate, which is renally excreted

Front 23

What happens in hemoglobinopathies (methemoglobin, CO poisoning)

Back 23

tissue hypoxia from decrease O2 saturation and decrease O2 content
Decreased O2 unloading

Front 24

What gases are perfusion limited in pulmonary circulation

Back 24

O2 (normal conditions), N2O, CO2

gas equilibrates early along capillary length
diffusion can be increased only if blood flow increases

Front 25

What gases are diffusion limited in pulmonary circulation

Back 25

O2 (emphysema, fibrosis), CO

gas does NOT equilibrate by the time blood reaches the end of the capillary

large partial pressure difference b/w alveolar air and pulmonary capillary blood

Front 26

What is primary pulmonary HTN

Back 26

due to an inactivating mutation in BMPR2 gene (normally functions to inhibit vascular smooth m proliferation); poor prognosis

Front 27

What are secondary causes of pulmonary HTN

Back 27

COPD, mitral stenosis, recurrent thromboemboli, autoimmune dz, L-to-R shunt, sleep apnea or living at high altitude

Front 28

What is the course of pulmonary HTN

Back 28

severe respiratory distress -> cyanosis and RVH -> death from decompensated cor pulmonale

Front 29

What are normal pulmonary artery pressure?

What are the values for pulmonary HTN?

Back 29

NL: 10-14 mmHg

HTN: >25 mmHg or > 35 during exercise

Front 30

What happens to O2 levels when Hb decreases?

Back 30

O2 content of arterial blood decreases

O2 saturation and arterial PO2 do NOT decrease
O2 saturation is determined by the amt of Hb

Front 31

What is the alveolar gas equation

Back 31

PAO2 = 150 - (PACO2/0.8) (approx)

actual: PAO2 = PIO2 - (PACO2/R)

Front 32

What is an A-a gradient?

List ddx for increased A-a gradient.

Back 32

PAO2 - PaO2 = 10-15 mmHg

V/Q mismatch, physiological shunt (airway block), R--> L shunt, fibrosis (diffusion block)

Front 33

What happens to PaO2 and PaCO2 during exercise? How does the body produce this result?

Back 33

PaO2 and PaCO2 stay the same

Vasodilation in the apex --> V/Q =1 in the apex --> less physiological dead space

Front 34

What can cause hypoxemia

Back 34

decreased PaO2

high altitude (NL A-a gradient)
Hypoventilation (NL A-a gradient)
V/Q mismatch (increased A-a gradient)
Diffusion limitation (increased gradient)
R-to-L shunt (increased gradient)

Front 35

What can cause hypoxia

Back 35

decreased O2 delivery to tissues

decreased CO
hypoxemia
anemia
CN poisoning
CO poisoning

Front 36

What can cause ischemia

Back 36

loss of blood flow

impeded arterial flow
reduced venous drainage

Front 37

Describe V/Q at apex and at base

Back 37

apex (zone 1): V/Q high ( = 3), wasted ventilation, high alveolar pressure compressed capillaries
PA > Pa > Pv (PA = alveolar pressure)

base (zone 3): V/Q low (= 0.6), wasted perfusion, Pa > Pv > PA, both ventilation and perfusion are greater at the base of lung than at the apex, but the proportionate increase of perfusion is greater than ventilation

Front 38

What happens when V/Q -> 0?

What happens when V/Q --> infinity?

Back 38

V/Q = 0
airway obstruction (shunt)
100% O2 does NOT improve PO2

V/Q = infinity
blood flow obstruction (physiological dead space)
100% O2 does improve PO2

Front 39

How does the body compensate for pH change in high altitude?
What drug can augment this effect?

pH change during exercise?

Back 39

high altitude
Hyperventilation --> low Pco2 --> respiratory alkalosis
compensation by renal HCO3- excretion
Can augment with acetazolamide

Exercise: lactic acidosis

Front 40

What is Haldane effect?

Back 40

Unloading of CO2 from RBC in the lungs

in lungs, oxygenation of Hb promotes dissociation of H+ from Hb,
this shifts equilibrium towards CO2 formation, releasing CO2 from RBC

Front 41

What is Bohr effect?

Back 41

Loading of CO2 to the RBC in the periphery
in peripheral tissue, increase H+ from tissue metabolism shifts curve to right, unloading O2

Front 42

What is carbaminohemoglobin

Back 42

CO2 bound to Hb at N terminus of globin, NOT heme

Front 43

What is Virchow's triad

Back 43

1. Stasis
2. Hypercoagulability
3. Endothelial damage

Front 44

What is Homan's sign

Back 44

DVT sign
dorsiflexion of foot -> tender calf m

can prevent w/heparin

Front 45

What is the hallmark sign for COPD

Back 45

decreased FEV1/FVC ratio (FEV1 decreases more than FVC)

Front 46

Curschmann's spirals

Back 46

shed epithelium form mucous plugs w/asthma in COPD

Front 47

What is centriacinar emphysema

Back 47

caused by smoking

Front 48

What is panacinar emphysema

Back 48

alpha1-antitrypsin deficiency (also liver cirrhosis)

Front 49

paraseptal emphysema

Back 49

assoc w/bullae -> can rupture -> spontaneous pneuomthorax

often in young, otherwise healthy males

Front 50

What are the clinical findings in emphysema in COPD

Back 50

dyspnea, decreased breath sounds,
tachycardia, late-onset hypoxemia due to eventual loss of capillary beds (w/loss of alveolar walls), early onset dyspnea

Front 51

What are the clinical findings in chronic bronchitis in COPD

Back 51

wheezing, crackles, cyanosis (early-onset hypoxemia due to shunting), late-onset dyspnea

"blue bloaters" (stocky and obese)

Front 52

What is bronchiectasis in COPD

Back 52

chronic necrotizing infection of bronchi -> permanently dilated airways, purulent sputum, recurrent infections, hemoptysis

Front 53

What conditions can cause bronchiectasis

Back 53

bronchial obstruction, CF, poor ciliary motility, Kartagener's syndrome

can get aspergillosis

Front 54

What disease states can cause restrictive lung dz

Back 54

1. Poor breathing mechanics (extrapulmonary):
poor muscular effort (polio, myasthenia gravis), poor structural apparatus (scoliosis, morbid obesity)

2. Interstitial lung dz: ARDS, neonatal RDS, pneumoconioses, sarcoidosis, idiopathic pulmonary fibrosis, Goodpasture's, Wegener's, Eosinophilic granuloma (Histiocytosis X), Drug toxicity (Bleomycin, busulfan, amiodarone)

Front 55

What is idiopathic pulmonary fibrosis

Back 55

repeated cycles of lung injury and wound healing w/increased collagen

Front 56

What are the main pneumoconioses

Back 56

Coal miner's, silicosis, asbestosis

Front 57

Silicosis

Back 57

"eggshell" calcification of hilar lymph nodes, macrophages respond to silica and release fibrogenic factors -> fibrosis

silica might impair macrophages, increasing susceptibility to TB

foundries, sandblasting, mines

Front 58

Coal miner's pneuomoconioses

Back 58

affects upper lobes, can result in cor pulmonale and Caplan's syndrome (combo of Rheumatoid nodule and pneumoconioses that manifest as intrapulmonary nodules)

Front 59

asbestosis

Back 59

"ivory-white," calcified pleural plaques

asbestos bodies in macrophages: golden-brown, fusiform rods that look like dumbbells

benign calcific plaques do not lead to cancer; must accompanied with interstitial fibrosis

increased incidence of bronchogenic CA (more common) and mesothelioma

Front 60

When is surfactant made in fetus

Back 60

most abundantly made after 35th week of gestation

Front 61

neonatal RDS

Back 61

lecithin:sphingomyelin ratio < 1.5
persistently low O2 tension -> risk for PDA, therapeutic supplemental O2 can cause retinopathy of prematurity

Front 62

What are the risk factors for neonatal RDS and do you treat it

Back 62

Risk factors: prematurity, maternal diabetes (b/c of high insulin), C-section (decrease release of fetal glucocorticoids)

Trx: maternal steroids BEFORE birth, artificial surfactant for infant, thyroxine

Front 63

Pathogenesis of ARDS

Back 63

diffuse alveolar damage -> increased alveolar capillary permeability -> protein-rich leakage into alveoli -> hyaline membrane

initial damage from neutrophilic substances toxic to alveolar wall, activation of coagulation cascade, or O2-derived free radicals

Front 64

What can cause ARDS

Back 64

trauma, sepsis, shock, gastric aspiration, uremia, acute pancreatitis, aminotic fluid embolism

Front 65

obesity, loud snoring, systemic/pulmonary HTN, arrhythmias, and possibly sudden death

What condition?

Back 65

Sleep apnea

Front 66

Central sleep apnea vs obstructive sleep apnea?

Back 66

central: no respiratory effort

obstructive: respiratory effort against airway obstruction

Front 67

What conditions cause an exudate in a pleural effusion

Back 67

malignancy, pneumonia, CVD (collagen vascular dz), trauma (occur in states of increased vascular permeability, like ARDS)

must be drained in light of risk of infection

Front 68

Transudate pleural effusion

Lymphatic pleural effusion

Back 68

Transduate: due to CHF, nephrotic syndrome, or hepatic cirrhosis (less albumin)

Lymphatic: milky fluid, increased triglycerides; due to obstruction to thoracic duct

Front 69

Lobar pneumonia: characteristics and organisms

Back 69

intra-alveolar exudate -> consolidation, can involve entire lung

orgs: Pneumococcus most frequently, Klebsiella

Front 70

Bronchopneumonia: characteristics and organisms

Back 70

acute inflammatory infiltrates from bronchioles into adjacent alveoli,
patchy distribution of >1+ lobes

orgs: S. aureus, H. flu, Klebsiella, S. pyogenes

Front 71

Interstitial/atypical pneumonia: characteristics and organisms

Back 71

diffuse patchy inflammation localized to interstitial areas at alveolar walls, involves >1+ lobes,
more indolent course than bronchopneumonia

orgs: Viruses (RSV, adeno), Mycoplasma, Legionella, Chlamydia

Front 72

What is a characteristic finding on X-ray for lung cancer

Back 72

pneumonic "coin" lesion

Front 73

what does primary lung cancer in lung present with?

How about metastasis to lungs?

Back 73

primary: cough

Metastasis: dyspnea

Front 74

What are the complications that can happen w/lung cancer

Back 74

SPHERE:
Superior vena cava syndrome
Pancoast's tumor
Horner's syndrome
Endocrine (paraneoplastic)
Recurrent laryngeal Sx (hoarseness)
Effusions (pleural or pericardial)

Front 75

What lung cancer type has PTHrp/parathyroid-like activity

Back 75

squamous cell CA

Front 76

What lung cancer types are found more centrally?

Peripheral?

Back 76

central: squamous and small cell

Peripheral: large cell and adenocacinoma (bronchial and bronchoalveolar)

Front 77

What is the most common lung cancer in women and nonsmokers

Back 77

adenocarcinoma

Front 78

List 3 paraneoplastic syndromes of small cell lung carcinoma.

Back 78

ACTH production: Cushing's sydnrome

ADH production: hypertension

Lambert-Eaton syndrome (autoabs to Ca channels)

Front 79

What histology is seen w/adenocarcinoma

Back 79

Clara cells -> Type 2 pneumocytes, multiple densities on CXR

Front 80

What is the consequence of bronchioloalveolar adenocarcinoma

Back 80

hypertrophic osteoarthropathy

this type of cancer grows along airways and can present like pneumonia

Front 81

What cancer is a neoplasm of neuroendocrine Kulchitsky cells and what are they?

Back 81

small dark blue cells

found in small cell CA

Front 82

what is carcinoid syndrome

Back 82

flushing, diarrhea, wheezing, salivation and R valvular heart dz

can be from a carcinoid tumor

Front 83

What is Pancoast's tumor?

Back 83

carcinoma in the apex of the lung and may affect cervical sympathetic plexus, causing Horner's syndome

Front 84

What lung abnormality?

absent or decreased breath sounds
decreased resonance
decreased fremitus
tracheal deviation toward the affected side

Back 84

bronchial obstruction

Front 85

What lung abnormality?

decreased breath sounds
dull resonance
decreased fremitus
no tracheal deviation

Back 85

pleural effusion

Front 86

What lung abnormality?

May have bronchial breath sounds over lesion
dull resonance
increased fremitus
no tracheal deviation

Back 86

lobar pneumonia or bronchiololalveolar adenocarcinoma of the lung

Front 87

What lung abnormality?

decreased breath sounds
hyperresonant
absent fremitus
tracheal deviation away from the affected side

Back 87

tension pneumothorax

Front 88

What group of bacteria is commonly aspirated?

What group of people is it commonly seen in?

complication?

Back 88

Anaerobes or S aureus; also Peptostrep and furobacterium

common in pts prediposed to loss of consciousness (alcoholics or epileptics)

can lead to lung abscess

Front 89

Describe 4 stages of gross changes in lobar pneumonia

Back 89

1. congestion: red, heavy, boggy lobe; vascular dilation, bacterial alveolar exudate
2. Red hepatization (2-3 days): red, firm lobe; RBC, neutrophils, and fibrin in alveolar exudate
3. gray hepatization (4-5 days): gray-brown lobe; neutprhils, fibrin and disintegrated RBC in alveolar exudate
4. resolution: restoration of normal architecture; enzyme digestion of exudate

Front 90

Diphenhydramine, dimenhydrinate, chlorpheniramine

class?
Indications?
toxicity?

Back 90

first generation H1 blockers

used for allergy, motion sickness, sleep aid
toxicity: sedation, antimusarinic, and anti-alpha adrenergic

Front 91

Loratadine, fexofenadine, desloratadine, cetririzine


class?
Indications?
toxicity?

Back 91

2nd gen H1 blockers

used for allergy

far less sedating than 1st gen b/c decreased entry to CNS

Front 92

Isoproterenol

class
Indication
MOA
adverse effects

Back 92

asthma drug
nonspecific beta agonists

relaxes bronchial smooth muscle
can cause tachycardia

Front 93

Albuterol, salmeterol

class
Indication
MOA

Back 93

asthma drugs

relaxes bronchial smooth muscle
Albuterol: for acute attacks
Salmeterol: for prophylaxis

Front 94

theophylline

class
Indication
MOA
adverse effects

Back 94

asthma drug
methylxanthines

inhibit phosphodiesterase --> high cAMP

narrow therapeutic index due to cardiotoxicity and neurotoxicity

Front 95

Ipratropium

class
Indication
MOA
adverse effects

Back 95

asthma drug
muscarinic antagonists

prevent bronchoconstriction and COPD

Front 96

Cromolyn

class
Indication
MOA
adverse effects

Back 96

asthma drug

prevent release of mediators fro mast cells
only for prophylaxis of asthma

Front 97

Beclomethasone, prednisone as asthma drugs.

MOA
indication

Back 97

corticosteroids

inhibit all cytokines by inactivating NF-kB --> no TNF alpha

first line of therapy for chronic asthma

Front 98

Zilueton

class
MOA
indication

Back 98

asthma drug
Antileukotrine

block 5-lopoxygenase --> no leukotrine production

Front 99

Zafirlukast, montelukast

class
MOA
indication

Back 99

Asthma drugs
antileukotrines

block leukotrine receptor (LTC4, LTD4, LTE4)
good for aspirin induced asthma

Front 100

Guaifenesin (Rubitussin)

N-acetylcystine

Indication
MOA

Back 100

Guaifenesin: removes excess sputum but large doses necessary; does not suppress cough reflex

N-acetylcystine: mucolytic --> can loosen mucous plugs in CF pts. also used as an antidote for acetaminophen overdose

Front 101

Bosentan

indication
MOA

Back 101

for pulmonary HTN

competitively antagonizes endothelin-1 receptors, decreasing pulmonary vascular resistance