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108 Cards in this Set

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What types of organisms do you see with lobar pneumonia? bronchopneumonia? how about interstitial?
Lobar: Pneumococcus most frequently; you see an intra-alveolar exudate with consolidation that may affect the whole lund

Bronchopneumonia: S. Aureus, H. flu, Klebsiella, S. pyogenes--> patchy distribution involving one or more lobes; infiltrate from the bronchioles into the adjacent alveoli

Interstitial (atypical pneumonia): caused by viruses (RSV and Adenoviruses) Mycoplasma (walking pneumonia) legionella and chlamydia--> these is diffuse patchy inflammation, localized to the interstialy areas at alveaolar walls. Usually a more indolent course than bronchopneumona--X ray looks worse than the patient does
What are the H1 blockers?
First generation: diphenhydramine, dimenhydrinate, chlorpheniramine--- these have sedating effects, used for allergy, motion sickness and as a sleep aid

Toxicity: sedation, antimuscarinic and anti-alpha adrenergic

Second Generation: Loratidine, Fexodenadine, Desloratiadine, Cetirazine-- are much less sedating because of decreased entry into the CNS, still used for allergy
What are some asthma drugs used to treat prophylactically?
Cromolyn, Nedocromil: prevents the release of mast cells; not effective in an acute attack

Zafirlukast and Montelukast: Block the Leukotriene (D4) receptor to prevent inflammatory mediators
How does theophylline (methylxanthine) work?
It is a phosphodiesterase inhibitor that causes bronchodilation by inhibiting phosphodiesterase, causing a decrease in cAMP hydrolysis

narrow therapeutic index, cardio and neurotoxicity, cyt p450 metabolism
How does Ipratropium work?
It is a competitive Muscarinic antagonist, which prevents bronchoconstriction

also used for COPD
what is first line therarpy for chronic asthma?
Corticosteroids

beclomethasone and prednisone--> these inhibit the synthesis of all cytokines, inactivate NFKappaB which induces the production of TNF alpha
What are some expectorants?
Guaifenesin (robitussin) which removes excess sputum, but a large dose is necessary--> does NOT suppress the cough reflex

N-acetylcysteine (Mucormyst) can loosen mucous plus in CF patients, and also used as an antidote for tyelenol overdose
why not give oxygen rapidly to a COPD patient?
chronic hypercapnia causes hypoxia to be the main respiratory stimulus (whereas normal people use increase pCO2 as the stimulus) so, high doses of Oxgen quickily may cause respiratory failure
How does one present with lung cancer?
hemoptysis, bronchial obstruction, wheezing, pneumonic coin lesions on X-ray film

mets to the lung are most common (breast) presents with dyspnea

primary in the lung presents with a cough
What are the complications associated with Lung Cancer?
SPHERE

Superior Vena Cava Syndrome
Pancoast's Tumor
Horner's Syndrome
Endocrine (paraneoplastic)
Recurrent Laryngeal Symptoms (hoarseness)
Effusions (pleural or pericardial)
What lung cancers occur centrally? peripherally?
central: squamous and small cell (oat cell)

Peripheral: adenocarcinoma, large cell carcinoma
What lung cancer may lead to lambert eaton syndrome?
Small Cell--> also often associated with ACTH or ADH release

Lambert Eaton: autoantibodies against Ca++ channels

Small cell carcinoma: has kulchitsky cells--> small blue, dark cells
what does the FEV1/FEV look like in obstructive lung disease
obstructive: less than 80%

restrictive: you'd see either normal (80%) or high (more than 80) FEV1/FEV
What are some obstructive lung diseases?
chronic bronchitis, emphysema, asthma and bronchiectasis

you see a decreased FEV1/FVC ratio

you have a hard time expiring-- remember you have super high compliance, making inspiration easy, but no recoil to expire, causing air trapping
What is responsible for surfactant production from the type II pneumocytes?
Cortisol from both mom and baby, stimulates surfactant production

L:S ratio of more than 2 indicates fetal lung maturity
Clara Cells
nonciliated columnar, with secretory granules. secrete component of surfactant; degrade toxins and act as reserve cells
Where should you look if you've aspirated a peanut while sitting up? while laying down?
upright, lower inferior lobe, right side

Supine, superior portion of right inferior lobe
What structures, and at what levels do they pierce the diaphragm?
T8: IVC
T10: esophagus, vagus
T12: aorta, thoracic duct, azygous vein

I ate 10 eggs at noon (12)
What are the muscles of respiration? During quiet breathing, during exercise?
Quiet Breathing: inspiration is active (diaphragm), expiration is passive

Exercise: Inspiration: external intercostals, scalene muscle and sternomastoids
Expiration: rectus abdominus, internal and external obliques, transversus abdominus, internal intercostals
Hypoxemia of Pulmonary Origin
Increased A-a gradient

whereas extrapulmonary has normal A-a gradient
Calculation of A-a gradient
PA02= Percent Oxygen (713) - arterial PCO2/.8

(.21)*713-(40*1.2)=100mmHg PA02
What is the normal Pa02?
95mmHg

so the normal A-a gradient is 100-95=5mmHg

Medically significant A-a gradients are more greater than or equal to 30
Medically significant A-a gradients?
>30
Causes of hypoxemia with an increased A-a gradient
Ventilation Defect (airway collapse)
Perfusion Defect (PE)
Diffusion Defect (Interstitial Fibrosis, or Edema)
Right to Left Cardiac Shunts (Tetralogy of Fallot)
Nocturnal Cough
GERD due to acid reflux into the bronchial tree at night or Bronchial Asthma: bronchoconstriction
Productive Cough
Chronic Bronchitis (smoking)
Bacterial Pneumonia
Bronchiectasis
Drugs that cause a cough
ACE inhibitors: inhibit the degradation of bradykinin causing mucosal swelling and irritation in the bronchial tree

Aspirin: causes an increase in LT-C-D-E4 (bronchoconstrictors)
What is the most common cause of hemopytis?
Chronic Bronchitis
What are some causes of hypoxemia with normal A-a gradients?
respiratory depression (barbiturates or brain injury)
Paralyzed diaphragm or ALS (anterior horn degeneration)
Upper airway blockage (food, epiglottisis (H. flu) Croup (parainfluenza)
What lung volumes and capactities cannot be measured by spirometry?
Residual Volume, Total Lung Capacity and FRC

FRC: total amount of air in lungs after a normal expiration

RV: volume of air in the lungs after a MAXIMAL expiration

TLC: total amount of air in a fully expanded lung
what is tidal volume?
The volume of air entering and leaving the lungs with normal breathing
Forced Vital Capacity
the total amount of air expelled after a maximal inspiration; normal is 5 liters
FEV1
normal is 4 Liters

FEV1/FVC is normally around 80%

increased in restrictive diseases, decreased in obstructive
newborn turns blue when breastfeeding
choanal atresia

unilateral or bilateral bony septum between the nose and the pharynx
Nasal Polyps in a child
must rule out CF; order a sweat test--> nasal polyps are often associated with CF
What are the most common types of polyps?
Allergic Polyps--> most often seen in adults with a history of IgE mediated allergies
What drugs are associated with nasal polyps?
Aspirin and other NSAIDS

COX inhibititors leave the LOX open--> leukotrienes C, D, E4 are increased causing bronchoconstriction--> develop polyps
What complications are associated with OSA?
Cor Pulmonale-- Right Ventricular Hypertrophy and pulmonary hypertension

See respiratory acidosis during apneaic episodes
Sinusitis
Strep Pneumo is the most common pathogen causing sinusitis

maxillary: adults
ethmoid: children

sinusitis is most frequently caused by an URI; symptoms are caused by a blockage of drainage into the nasal cavity--> clinical findings include fever, pain over sinuses, nasal congestion
Nasopharyngeal Carcinoma
assocaited with EBV, squamous cell carcinoma or undifferentiated cancer. Mets to cervical lymph nodes
Laryngeal Carcinoma
Smoking is the most common cause, though alcohol is synergistic with smoking

HPV (6 and 11) association, and the majority of the tumors are on the TRUE vocal cords

keratinizing squamous cell carcinoma
Atelectasis
Loss of lung volume due to inadequate expansion of the airways (collapse)

1. Resorption: airway obstruction (most common cause of fever 24-36 days after surgery)
2. Compression: tension pneumothorax or pleural effusion
3. Loss of surfactant
Surfactant production
Cortisol and Thyroxine increase synthesis

Insulin inhibits synthesis

Thus, Maternal Diabetes may cause RDS, along with C-section where you don't have the stress-induced increase in cortisol due to vaginal delivery
What are some causes, and ways to check on metabolic alkalosis?
Loss of H ions (puking, NG suction)

Loss of Na+ followed by a loss of Cl- leading to reabsorption of HCO3-

Increased Aldosterone Secretion (reabsorb Na+, excrete K, H and Cl- with a relative increase in HCO3-)

Do a urine check of Cl- levels
What is the most common cause of pulmonary edema?
Left heart failure

Starling Forces causing Pedema
1. Can see mitral stenosis, volume overload leading to increased hydrostatic pressure

2. or see decreased oncotic pressure with cirrhosis or nephrotic syndromes

Injury
1. Infections (sepsis, pneumonia)
2. aspirations (drowning, gastric content)
3. Drugs (heroin) shock, massive trauma
4. High altitude
Pneumonia
Community Acquired or Nosocomial

CA: majority are bacterial (strep pneumo) that are inhaled from an infected pateints, or aspiration of nasopharyngeal flora while sleeping

Bronchopneumonia (acute bronchitis, and spreads locally to the lungs) or Lobar Pneumonia

Signs: fever and productive cough, signs of consolidation

Atypical CA-pneumonia often times mycoplasma pneumonia-- patchy interstitial pneumonia, NO signs of consolidation
How would you distinguish clinically signs of typical pneumonia from atypical pneumonia
Atypical you don't see any signs of consolidation because it's generally interstitial, the alveolar are free of exudate

typical pneumonia (s. pnuemo) you have consolidation (dullness to percussion, increased vocal tactile fremitus, sound is better transmitted through consolidations
Nosocomial Pneumonia
Epidemiology: severe underlying disease, antiobiotic therpay, immunosuppression. Most commonly comes from respirators

Pathogens are gram negative bacteria (pseudomonas aeruginosa--respirators) or E. Coli

Gram Positive bacteria are Staph Aureus
pneumonia in immunocompromised patients
CMV
Pneumocystisis Jiroveci
Asperigillus Fumigatus

you treat pneumocystis jiroveci with TMP-Sulfa for prophylacxis treatment
TB
PPD does NOT distinguish an active from an inactive infection

kidneys are the most common extrapulmonary site of TB infection
Klebsiella Pneumonia
Gram Negative fat Rod surrounded by a mucoid capsule

common cause of pneumonia in alcoholics, however s. pneumo is still the msot common pneumonia

Currant Red sputum
psuedomonas aeruginosus
green sputum (pyocyanin) gram negative fat rod covered with a capsule, water loving (most frequent cause of nosocomial pneumonia on respirators)

also most frequent cause of death to pneumonia in CF patients
Legionella Pneumophilia
gram negative rod

water loving (water coolers, mists in the produce section, rainforests in zoos)

may produce tubulointerstitial disease with destruction of the JGA leading to hypoaldosterone and hyporeninin
myocplasma
military recruits, adolescents small confined areas

walking pneumonia

insidious onset with low grade fever, may see cold agglutinins in the blood
Nonspecific beta agonists
Isoproterenol: relaxes bronchial smooth muscle (beta 2) but adverse effect is tachycardia (b1)
Beta 2 agonists
Albuterol and Salmeterol: salmeterol is longer acting, whereas albuterol is used during an acute exacerbation

albuterol relaxes bronchial smooth muscle, salmeterol's adverse effects are tremor and arrhythmia
Theophylline
INHIBITS PHOSPHODIESTERASE, thereby decreasing cAMP hydrolysis

usage is limited due to narrow therapeutic index (cardio and neurotoxicty) metabolized by P-450
Ipratropium
Competitive block of muscarinic receptors, preventing bronchoconstriction--> also used for COPD

iptratropium requires parasympathetics--> it is just blocking the constriction. So without a vagus nerve, you've got no working ipratropium
5-lipoxygenase inhibitor
Zileuton

blocks conversion of arachianic acid into leukotrienes
Bosentan
blocks endothelin, which is a potent vasoconstrictor that stimulates endothelial proliferation

used in the tx of primary pulmonary hypertension
hering breur reflex
regulates lungs distension, affects the duration of inspiration and expiration, via the myelinated and unmyelinated C fibers in the lungs
bronchial obstruction
absent or decreased breath sounds of the affected area

the trachea will deviate TOWARD the side of the lesion

decreased resonance and decreased fremitus
barrel shaped chest
emphysema, where you have increased compliance, and less of a lung's tendency to collapse. Thus, the chest wall will have an increased tendency to expand--> higher FRC

Air trapping
What is vital capacity?
TV + IRV + ERV

so it's total lung capacity, minus the residual volume
What is tidal volume?
about 500 ml, the air that moves in and out of the lung with each breath
what are some important lung products?
Surfactant
Prostaglandins
Histamine
ACE (which inactivates bradykinin, which explains why ACEInhibitors increase bradykinin and cause cough, angioedema)
Kallikrein (which activates bradykinin)
Collapsing Pressure
2 (tension)/ radius

tendency to collapse on expiration as radius decreases
What is the role of ACE and of kallikrein in the lung?
ACE inactivates bradykinin and kallikrein activates it.
What is the physiological dead space?
Vd= Tidal Volume * (PaCO2-PeCO2)/PaCO2

so it's the anatomical dead space of the conducting airways plus the functional dead space in the alveoli--> the apex of healthy lungs are the biggest contributor to functional dead space
Hemoglobin
2 alpha and 2 beta chains, existing in 2 forms

taut: not much affinity for O2
relaxed: high affinity for O2
fetal hemoglobin
has lower affinity for 2,3 BPG than adult hemoglobin, and thus higher affinity for O2
Right shifting the Oxygen Dissociation Curve
Increased temperature, Cl-, H+, 2,3 BPG, and CO2 all favor the taut form more so than the relaxed form--> which means there is a lower affinity for Oxygen, and it'll unload at the tissues
methemoglobin
has increased affinity for CN-

Iron in the Ferric State (Fe3+)

Treat with metheylene blue
How do you treat Cyanide Poisoning?
use nitrites to oxidize hemoglobin to methemoglobin (Fe3+), which binds cyanide, allowing cytochrome oxidase to function; Use thiosulfate to bind this cyanide, forming thiocyanate, which can be renally excreted
What does altitude do to the oxygen dissociation curve?
shifts it RIGHT

along with CO2, Acid, DPG, exercise and Temperature
In what conditions are the lungs diffusion limited?
emphysema, fibrosis
pulmonary hypertension
normal pulmonary artery pressure is around 10-14 mmHg

In Pulmonary HTN: is more than 25 mmHg or 35 during exercise

results in atherosclerosis, medial hypertrophy, intimal fiborsis of the pulmonary arteries

PRIMARY: due to inactivating mutation in BMPR2 gene (normally functions to inhibit smooth muscle proliferation)
BMPR2
gene mutated in primary pulmonary HTN

BMPR2 normally inhibits vascular smooth muscle proliferation
Secondary Pulmonary HTN
due to COPD, mitral stenosis, recurrent thromboemboli, autoimmune disease, left to right shunt, or sleep apnea

the course: severe respiratory distress which leads to cyanosis and RVH and death from decompensated cor pulmonale
Coccidiodes Imitis
Spherule filled with endospores

San Joaquin Valley-- or desert bumps, valley fever

See erythema nodosum, or subcutaneous nodules, flu like symptoms
Narrow Based Buds
Cryptococcus

seen with bat droppings
Broad Based Buds
Blastomycosis

see skin and bone-- and the skin lesions simulate squamous cell carcinoma
What do you see with bat droppings?
cryptococcus neoforms and histoplasmosis

crypto: narrow based buds
Histo: yeast filled macrophages
Dimorphic Fungi
mold in soil
yeast in tisuue

Histo, Blasto, Paracoccidio

Coccidio: is not a yeast in tissue, but rather a spherule

all of these may cause pneumonia, and may disseminate

treatment: fluconazole or ketoconazole for local infections, and amphotericin B for systemic infections
Mycoplasma Pneumonia
Walking Pneumonia--> insidious onset, nonproductive cough, diffuse interstitial infiltrate

X ray looks worse than the picture; high titers of cold agglutinin (IgM)

NO cell wall, not seen on gram stain; it's the only bacterial membrane containing cholesterol

treat: tetracycline or erythromycin

mycoplasma is penicillin resistant because they don't have a cell wall

mycoplasma is grown on Eaton's Agar
Opportunistic Fungal Infections
Asperigillus (45 degree branching hyphae (colonizing, invasive and allergic)

Candida: yeast with pseudohyphae in culture at 20, germ tube formation at 37 is diagnostic

(tx candida with nystatin for superficial, and amphotecerin B for disseminated)

Cryptococcus Neoformans (narrow based buds, NOT dimorphic) latex agglutination detects polysaccaride capsule, soap bubble in brain

Mucor and Rhizopus--> these are mold with irregular septae with wide branching angles, seen in DKA and leukemic patients
Wide-branching angle of irregular septae
Mucor and Rhizopus Species

this is mold with irregular septae, seen in Leukemics and DKA. fungi may proliferate in blood vessels, causing infarction--> rhinocerebral frontal lobe abscess
Pneumocystis Jirovecii
Causes diffuse interstitial pneumonia, most are aymptomatic unless immunocompromised. Diffuse bilateral CXR appearance

Dx: methenamine silver stain of the lung tissue

Tx: TMP-SMX, pentamidine, dapsone

Start prophylactic treatment when CD4 counts drop below 200 cells in HIV patients

cysts look like crushed ping pong balls-- NEED silver stain
How do you treat sporothrix schenckii
-- Cigar shaped budding yeast are visible in the pus

Treat with potassium Iodide (KI) or Itraconozaole
Lab Findings with Pulmonary Infarction
Respiratory Alkalosis (arterial PCO2 is less than 33)

PaO2 is less than 80 mm Hg
A-a gradient is INCREASED in all cases
Abnormal Perfusion radionuclide Scan-- where the ventilation is normal, but the perfusion scan is abnormal
Positive D-Dimers
What clinical signs are consistent with pulmonary hypertension
Accentuated P2
Progressive Dyspnea and Chest Pain with exertion
Left parasternal heave indicative of RVH
Right Sided Failure due to Cor Pulmonale
Goodpasture's Syndrome
Pulmonary Hemorrage with hemoptysis generally precede renal failure

you will see a linear pattern on EM of the kidney-- it's an anti-body against the noncollagenous alpha 3 chain of Collagen IV (type II hypersensitivity)
Interstitial Lung Diseases
Pneumoconioses
Goodpasture's
ARDS
Sarcoidosis
Hyaline Membrane Disease
Wegener's
Eosinophilic Granuloma (histiocytosis X)
Drug Toxicity (bleomycin, amiodarone, busulfan)
Silicosis
Most common occupational disease in the world

Quartz (crystalline silicone dioxide) most often implicated

Foundries, Sandblsting, working in mines

quartz is highly fibrogenic, deposits in the upper lungs--> quartz activates
How do you calculate the PAO2?
150-Pco2/0.8

.8 is the respiratory quotient
What are some causes of hypoxemia with increased A-a gradient
they are intrapulmonary problems

ventilation defect
perfusion defect
diffusion defect
Right to Left shunt
Hypoxemia with a normal A-a gradient
Respiratory Depression or Upper airway obstruction
Chest Dysfunction
resorption atelectasis
airway obstruction prevents air from reaching alveoli

generally from mucous plug after surgery, aspiration of foreign material, or centrally located bronchogenic carcinoma

clinical findings: fever and dyspnea, absent breath sounds and focal fremitus, ipsilateral elevation of the diaphragm and tracheal deviation-> inspiratory lag
Compression atelectasis
Increased pressure causes the lung to collapse

tension pneumothorax and pleural effusion

trachea will deviate away from the collapsed lung
typical community acquired pneumonia
due to strep pneumo

alpha hemolytic, optochin sensitive--> strep pneumo is also a competent bacteria capable of taking up DNA from other bacteria that have died
patchy areas of consolidation in the lungs full of neutrophils in the alveoli and bronchi
Bronchopneumonia

begins as an acute bronchitis, and then spreads locally into the lungs
What is the most common cause of atypical pneumonia?
mycoplasm pneumonia
What causes nosocomial pneumonia; contracted from respirators?
Pseudomonas Aeruginosus
what is the most frequent cause pulmonary thromboembolism?
femoral veins--> 95%
Restrictive Lung Disease
Decrease of ALL lung volumes and capacities

decreased FEV1, but decreased FVC leads to an increased ratio

often have the FVC the same as the FEV1 due to the increased lung elasticity
Silicosis
quartz is most often implicated

in the upper lobes of the lung, it is highly fibrogenic. See eggshell calcifications and birefrigent particles surrounded by fibrous tissue
What complications are you at risk for in devloping pneumoconiosis?
TB and lung cancer. Cor pulmonale and caplan syndrome (RA nodules in the lung + a pneumoconiosis)
unexplained pleural effusion in a young woman?
SLE until proven otherwise