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175 Cards in this Set

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What is contained with in the "conducting zone" of the respiratory tree? Function??
Conducting zone:

Nose, pharnyx, trachea, bronchi, bronchioles, and terminal bronchioles.

Function: brings air in and out; warms and humidifies, filters air.

Aka: anatomical dead space

What are the walls of the conducting airway lined with?
Smooth muscle

What is contained with in the "respiratory zone"

Respiratory bronchioles, alveolar ducts, and alveoli

Function: gas exchange

What is the epithelium lining the areas of the lung?
Pseudocolumnar ciliated cells extend to the respiratory bronchioles.

Goblet cells extend only to the terminal bronchioles.

Type I cells (93%) line the alveoli and type II line 3% and secrete surfactant.

Function of surfactant?
Surfactant: decreases surface tension of alveoli

What is special about type II pneumocytes? (3)
They serve as precursors to type I cells and other type II cells.

Also they can proliferate during lung damage

What is the lecithin-to-sphingomyelin ratio in amniotic fluid that is indicative of fetal lung maturity?
> 2.0

What can be seen in EM that can ID type II pneumocytes?
Lamellar bodies (look like onions on their side)

What is the relationship between the left and right lung hilus and where the pulmonary artery is located?

Right lung: pulm artery is anterior

Left lung: pulmonary is superior

p.121 clinical anatomy

What is contained in a bronchopulmonary segment?
Bronchopulmonary segment:

Each segment has a tertiary bronchus and 2 arteries (pulmonary and bronchial) in the center. Veins and lymphatics drain along the borders.

"arteries run with airways"

How many bronchopulmonary segments are there in each lung?

What are the structures that perforate the diaphagm?
I 8 10 EGGs AT 12:

I: IVC @ 8th vertebrae (T8)

EsophaGus and vaGus: 10th (T10)

Aorta(red), Azygous(blue), and Thoracic duct (white): 12th T12

What innervates the diaphragm? What vertibrae are associated?
Phrenic nerve:
C3, 4, 5 (spinal nerves)

Where does referred pain from the diaphragm go to?

What are the muscles of inspiration/expiration on quiet breathing?
Inspiration: diaphragm

Expiration: passive

What are the muscles of respiration used during exercise?
1. external intercostals
2. scalene muscles
3. sternomastoids

1. rectus abdominis
2. internal and external obliques
3. transverus abdomnis
4. internal intercostals

What does surfactant do to compliance?
Increases it

What are the three names for surfactant?
1. Surfactant
2. dipalmitoyl phosphatidylcholine
3. lecithin

Five important products made in the lungs:
1. surfactant
2. prostaglandins
3. histamine (increase bronchoconstriction)
4. ACE to convert Angio I to Angio II and to inactivate bradykinin
5. Kallikrein: activates bradykinin and plasmin (to degrade fibrin clots)

What is the formula for collapsing pressure?
2(tension) / radius

Residual lung volume?
Air in lung after maximal expiration

"Resistant volume" - resists being forced out

Expiratory reserve volume (ERV)
Air that can still be breathed out after normal expiration (MOW: and that is breathed out after a large inspir/expir)

Tidal volume
Air that moves into lung with each quiet inspiration (typically 500mL)

Inspiratory reserve volume
Air in excess of tidal volume that moves into lung on maximum inspiration.

Vital capacity formula?

(everything but the residual volume)
"residual/resistant volume better not be VITAL or you are out of luck"

Functional reserve capacity?
FRC = RV + ERV (volume in lungs after normal expiration)

Inspiratory capacity?
The air in excess of tidal volume that moves into lung on maximum inspiration
(the TV to the highest peak)

Total lung capacity:
TLC = IRV + TV + ERV + RV (everything in the graph)

How would the tidal volume change in exercise? how would that also change the expiratory flow rate?
Exercise: increase TV

It also causes an increase in expiratory air flow rate because resp rate has increased greatly and max expiratory effort is required to move the 2.5L (nL: 0.5L) of tital volume out of the lung

What is the formula to determine the physiologic dead space? What does this formula resemble?
Formula for dead space:
Vd = Vt x ((PaCO2 - PeCO2)/ PaCO2)
Pe: expired air PCO2

Kind of resembles the formula for determining the A-a gradient:
PAo2 = PIo2 - (PAco2/R)
PI: inspired air
R: respiratory quotient
PA: alveolar

Patient exhibits an extended expiratory phase:
What is the disease process?
Obstructive lung disease

Tall, thin, male teenager has abrupt-onset dyspnea and left-sided chest pain. There is hyperresonant percussion on the affected side and breath sounds are diminished. Dx?
Spontaneous pneumothorax

(note: not atelectasis because of hyperresonance)

What happens when you are at an increased altitude? Chronic?
High altitude:
Decreased PaO2 --> decreased SaO2 --> decreased O2 able to get into tissues.

Bodies response: Hypervent --> Chronic hypervent -->
1. increase erythropoietin
2. increase hematocrit/hemoglobin
3. increase 2,3 DPG
4. increase mitochondria
5. increase renal E of bicarb to compensate for resp alkalosis (augment with acetazolamide)

All can lead to chronic hypoxic pulmonary vasoconstriction = RVH

What is the mneumonic for "right shift" of oxygen dissociation curve?
Right shift - CADET face right:
DPG (2,3 DPG)

During hypoxia what happens to the lungs vasculature?
In low PaO2 --> vasoconstriction shifts blood away from poorly ventilated regions of the lung to well-ventilated areas.

Four situations in which pulmonary circulatory gas exchage is diffusion limited?
Diffusion limited: gas does not equilibrate by the time blood reaches the end of the capillary

1. exercise
2. emphysema
3. fibrosis
4. CO

What is the normal pulmonary artery pressure? What is pulmonary HTN value?

What is the value during exercise?
10-14 mm Hg

Pulmonary hypertension: > 25mmHg

Exercise: >35

What is the most common secondary cause of pulmonary hypertension?

What is the formulat for pulmonary vascular resistance?
PVR = Ppulm art - PLatrium / CO

What is the normal Hgb amount in blood?
15 g/dl

What can the alveolar gas equation normally be approximated to?
PAo2 = 150 - PartCO2 / 0.8

What is a normal A-a gradient?
A-a: 10-15mmHg

Q-bank: Pt with P02=90, PCO2=19, pH 7.3. What is the cause?
A. hypoventilation
B. hypoxia induced hyperpnea
C. impaired diffusion of 02
D. primary resp acidosis
E. the P50 of O2-hemoglobin curve is less than normal
Calc A-a: PA02= 150-19 / 1 = 131
A-a=131-90=40 --> high!

Impaired diffusion of O2!
A. wrong - low Pco2 = hypervent
B. wrong, only severe hypoxia would cause vent to double.
D. resp acidosis: increase in Pco2
E. acidosis shifts O2 curve to the right --> pt pH: acidotic

In obstructive lung dz what will happen to the values of:
Diffusion capacity with CO

What happens in restrictive?
Obstructive: (emphysema)
TLC: increased
RV: increased (can't get it out)
TV: decreased
VC: decreased (since TLC is increased and so is VC)
FEV: decreased; FVC: decreased
FEV/FVC: decreased
Diffusion capacity with CO: decreased

In restrictive: all is decreased except FEV/FVC: nL to increased!

What is 90% of CO2 transported in the form of?

What is the Haldane effect?
The effect of oxygenation of hemoglobin promoting dissociation of CO2 from hemoglobin

While breathing into a spirometer which is the only one that would produce a (+) airway pressure of +30?

FRC, minimal vol(amt of air remaining in excised lung), residual vol, tidal vol, TLC?
Do this yourself-inhale to TLC and relax --> you will want to exhale

In nL lungs what is the ratio between physiologic and anatomical dead space? In death?
nL: they are equal

death: physio < anatomical

what is functional residual capacity?
The value at which the collapsing force on the lung is equal to the expanding force on the chest wall

During inspiration describe the alveolar pressure:
It is negative

Q: 12yo with aplastic anemia, which would be decreased?
a. 2,3 DPG
b. arterial pO2
c. CO
d. mixed venous O2
e. RBC H conc.
d. mixed venous O2: when o2 content of the arterial blood is decreased the loss of O2 to the tissues will cause the venous O2 tension to fall to lower than nL levels during rest and very low levels when exercise is attempted.

The rest would be increased except arterial PO2 would stay the same.

Describe fetal pulmonary resistance and what happens after birth?
Fetal pulmonary vascular resistance is very high because of generalized hypoxic vasoconstriction; as a result, blood flow thorugh the fetal lungs is low. With the first breath, the alveoli of the neonate are oxygenated, pulmonary vascular resistance decreases, and pulmonary blood flow increases and becomes equal to cardiac output (as occurs in adults).

Where is the V/Q ratio the highest? Where is the blood flow the highest?
Where is the ventilation the highest?
Where is the highest regional O2?
V/Q: apex

Ventilation: HIGHER in BASE
Blood flow: HIGHER in BASE
Highest regional O2: APEX

Describe the part of the central control of breathing that is the medullary respiratory center:
Meduallary respiratory center:
located in the reticular formation

Dorsal resp group: primarily responsible for inspiration and generates the basic rhythm for breathing. Input comes from the vagus and glossopharyngeal n. Output from the dorsal respiratory group travels via the phrenic nerve to the diaphragm.

Ventral resp group: primarily responsible for expiration. It is not active during normal quiet breathing when expiration is passive. It is activated though during exercise, when expiration becomes an active process.

What does the apneustic center do and where is it located?
Apneustic center: lower pons

Stimulates inspiration, producing a deep and prolonged inspiratory gasp.

What does the pneumotaxic center do and where is it located?
Pneumotaxic center: upper pons

Inhibits respiration and therefore, regulates inspiratory volume and respiratory rate.

What does the cerebral cortex do to control breathing?
Cerebral cortex:
breathing can be under voluntary control; therefore a person can voluntarily hyperventilate or hypoventilate.

Where are central and peripheral chemoreceptors located for breathing?
Central: medulla (sensitive to pH)

Peripheral: carotid and aortic bodies (sensitive to increase/decrease in pO2 and increases in arterial H)

What are J receptors and how to they control breathing?
J receptors: they are located in the alveolar walls, close to the capillaries.

Engorgement of the pulmonary capillaries such as may occur with left heart failure, stimulates these receptors which then cause rapid, shallow breathing.

Describe what happens to PO2, PCO2, arterial pH, ventilatory rate, pulmonary blood flow, and amount of dead space during exercise
Mean values for arterial PO2 and PCO2 do not change.
Arterial pH does not change during moderate exercise although it may decrease during strenuous exercise.

Pulmonary blood flow increases.
There was a decrease in the physiologic dead space.

What kind of hypersensitivity reaction is allergic rhinitis?
Type I (increased eosinophil count)

Most common cause of acute epiglottis?
H. influenzea

Can allergic polyps be seen in children?
NO!! if you are a kid with a nasal polyp = cystic fibrosis

What is triad asthma? Is this immune mediated?
When you get asthma from taking aspirin and you have a current nasal polyp

Not immune mediated: it is caused by aspirin blocking the cyclooxygenase so arachidonic acid can't form PGG2 and instead must become leukotrienes --> LTC,D,E4 cause bronchoconstriction

Most common cause of nasopharyngeal carcinoma?
EBV (Asia and east africa)

Singer's nodule
Benign nasal polyp associated with heavy cigarette smoking and is usually localized on the true vocal cords

What is the most common tumor of the larynx?
Squamous cell CA -- seen in men 40+ and assoc with smoking and alcohol

Presents after persistant hoarseness as arises from the true vocal cords

Where is the most common site of aspiration when standing or sitting?

Lying on back?
Standing or sitting: posterior basal segment of right lower lobe

Lying down: upper segment of right lower lobe

What symptoms would you have if you damaged your inferior laryngeal n. (recurrent laryngeal)?
Speech prob if both nerves
Breathing prob if both nerves

Most common causes of damage to recurrent laryngeal?
Thyroidectomy: close to inferior thyroid artery

Thoracic lesions in L recurrent laryngeal lesions

What are the TLC, FRC, RV, ad FEV1/FVC ratio in an obstructive lung disease?
all increased

except for FEV1/FVC: decreased since FEV1 is more dramatically reduced (can't get air out) than FVC

When do you see curshman spirals?

What are the TLC, FRC, RV, ad FEV1/FVC ratio in a restrictive lung disease?
All decreased except for ratio of FEV1/FVC = increased (airways are fibrosed: snap in retraction to get air out and thats it, don't get alot of air out but --> FEV1 = FVC)

Q: What happens to PO2, PCO2, and pH in COPD?

What mechanism does the body have to help this?
PO2: decreases
PCO2: increases
pH: decreases (but kidney can compensate for this - close to normal)

Kidney: metabolic alkalosis
BM: polycythemia

Compare intrinsic and extrinsic asthma:
Instrinsic: nonimmune, caused by asprin, chronic bronchitis, exercise, cold-induced (begins in adult life)

Extrinsic: type I hypersensitivity reaction involving IgE bound to mast cells (diseaes begins in childhood; family hx)

Where is the most common location of larnygeal sqamous cell carcinoma?
MC: supraglottic

Best prognosis: true vocal cords

What morphological findings in an asthma patient tell us the asthma is allergic?
Presence of eosinphils
Charcot-Leydig crystals (made by eosinophils -- seen in many allergic processes)

Describe the morphologic features in asthma:
1. hypertrophy of bronchial smooth m
2. hyperplasia of goblet cells
3. thickening and hyalinization of the basement membrane
4. prolif of eosinophils (if allergic)
5. intrabronchial mucus plugs
6. Curshmann spirals
7. Charcot-leydig crystals (if allergic)

Describe the allergic process in allergic asthma:
Type I hypersensitivity:
Th2 (CD4)cell activation by macro/dendrocite --> release of IL 4, 5, 6 --> IL4 tells Bcells to make IgE over IgG --> increased IgE directed against allergen --> IgE antibodies attach to mast cells --> allergen comes again --> binds to IgE--> increase mast cells degranulation --> causes bronchospasm

Q: how do viruses (infections) causes intrinsic (nonallergic) asthma?
Viral infection of URT can lower the threshold of resp mucosa to parasympathetic (vagal) stimulation --> vagus is stimulated more --> bronchoconstriction.

What happens to I/E ratio in asthmatics?
decreased I/E

what is needed to diagnose chronic bronchitis officially?

Clincial findings?
productive cough for > 3 consecutive months in > 2 yrs

Findings: wheezing, crackles, and cyanosis "blue bloater"

What enzyme is increased in emphysema?

in chronic bronchitis where is the dz specifically located?
In the terminal bronchioles (mucus blocks all the parellel branching that occurs at the terminal bronchioles where air flow is supposed to turn from turbulent to laminar)

Terminal bronchiole (mainly affected) is proximal to the respiratory unit

Compare emphysema and chronic bronchitis:

1. sputum production
2. onset of dyspnea
3. hyperinflation
4. PaCO2
1. sputum production: more in CB (scant in emphy)
2. emphy dyspnea: constant and progressive, severe; CB: intermittent and exaserbated with infection
3. more hyperinflation in emphy
4. PaCO2: emphy = nl to low = respiratory alkalosis
Chronic bronchitis = increased = resp acidosis = cyanosis

What is the ventilation to perfusion matching in emphysema and chronic bronchitis?
Matched losses of ventilation and perfusion in emphysema (destroy resp unit and blood supply)

Mismatch in chronic bronchitis since perfusion in not effect but ventilation is.

Centrilobular emphysema
Dilation of the respiratory bronchioles that is most often localized to the upper part of the pulmonary lobes.
The upper lobe respiratory bronchioles is the first place the smoke stops at --> calls neutrophils --> destruction.

Cause: smoking (which can also lead to panacinar from inactivation of AAT)

Panacinar emphysema
Dialation of the entire acinus including the alveoli, alveolar ducts, resp. bronchioles, and terminal bronchioles.

Goljan: lower lobe diseaes

Cause: deficiency of alpha-1-antitrypsin with functions to destroy elastase produced by neutrophils (this enzyme can be denatured in smokers)

What is paraseptal emphysema?
Associated with bullae in intralobular septum --> can rupture --> pneumothorax.

Often in young, healthy males

G: Given an x-ray: what do you need to see to dx emphysema?
Increased AP diameter and depressed diaphragm (from hyperinflation --> air pushes down on diaphragm)

What is the piZZ allele associated with?
Chr 14
The homozygous state is assoc with decreased activity of alpha-1-antitrypsin, panacinar emphysema, and liver cirrhosis (incodes for a protein that inhibits hepatic secretion)

What type of inhibitor is alpha-1-antitrypsin?
Serum protease inhibitor

What is the most common cause of bronchietasis? What is bronchietasis?
Cystic fibrosis

Bronchietasis: permenant abnormal dilation of bronchial walls along with inflammation and necrosis. Airways are filled to the brim with pus

How is Kartegenar's syndrome associated with bronchietasis:
Kartagener syndrome involves: sinusitis, bronchietasis, and situs inversus.

Bronchiectasis is caused from a mutation in dynein arms = no cilia.

Atelectasis: pathophys and 4 signs
Atelectasis: collapse of alveoli due to mucus blocking terminal bronchioles and distal reabsorption of air through pores of Kohn

4 findings: signs of consolidation
1. elevated diaphragm
2. increased tactile fremitus
3. decreased percussion (resonance)
4. chest lag on inspiration

Where is surfactant stored?
Lamellar bodies

Pathophys of Adult respiratory distress syndrome (ARDS)
Some trauma/drug/ pancreatitis/uremia causes alveolar capillary permeability causing leakage of protein-rich fluid into alveoli as well as neutrophils. These neutrophils release toxic substances to the alveolar wall and activate the coagulation cascade and form O2 radicals.
Neutros kill of pneumocytes --> decreased surfactant --> massive atelectasis. Also the neutros get into capillaries and put holes in lung --> leaky caps --> form hyaline = = = Interpulmonary shunting (massive ventilation defect)

Q: Pt with sepsis that has dyspnea for on day 1 --> Dx? What could happen by day 3? day 4?

3d: DIC
4d: death

What is the MCC of ARDS?
Endotoxic shock --> septic shock as from e.coli in an indwelling catheter

What are two massive ventilation defect disorders?
ARDS and neonatal resp distress syndrome (hyaline membrane disease)

What causes hyaline membrane formation in the lungs?
Degeneration of type II pneumocytes and leakage of fibrinogen --> congeals = hyaline membranes

MCC of resp distress in infant?

What is a common murmur since in babies with NRDS?
Machinery murmur from patent ductus arteriosis

What does surfactant prevent?
alveolar collapse on EXPIRATION (expire --> decrease radius --> increase tension (2T/r)

When does the lecthin increase in a fetus? What is the ratio compared to?
Lecthin: increases in the 33rd-35th week; bipassing sphingomyelin.

Letch:sphingo --> less than 1.5 in NRDS

Three predisposing factors to NRDS:
1. prematurity
2. maternal diabetes mellitus (increase insulin -> decrease surfactant)
3. cesarean sectionv(no increase in cortisol)

A baby from a diabetic mom that did not have good glycemic control will have what when they are born (otherthan the possiblity of NRDS)
Hypoglycemia (it was mom's glucose that was high)

USMLE: What can you give to mom to increase babies surfactant levels? (corticosteriods, though correct, was not an option)
Thyroxine(wouldn't give to mom)

Rx of baby with NRDS?
Postitive end-expiratory pressure ventilation (keeps airways open on expiration)
and put in alittle surfactant

Q: What causes esophageal atresia?
Posterior deviation of the tracheoesophageal septum that will result in aspiration pneumo in an infant

Q: Congenital pulm cysts
Multiple, located in lung periphery with/o connection to the bronchi. They are vulnerable to infection and rupture.

Q: Pulmonary sequestration
Extrapulmonary lung tissue supplied by systemic blood vessels rather than by pulmonary arteries.

Q: 3mth presents with 3d Hx fever, cough, and poor feeding. On exam baby is tachypnic and CXR shows bilateral patchy infiltrates:
Dx: resp syncytiovirus (most common cause of bronchiolitis and pneumonia in children <1 - outbreaks in winter and spring)

ssRNA (-), env
protein G on viral envelop allows virus to attach to cells
protein F allows fusion of infected cells

HY: What is Caplan's syndrome?
Rheumatoid nodules in lungs + coal workers pneumoconiosis (exposure to coal dust; decreased compliance and increased elasticity due to interstial fibrosis)

What is a pt with coal miners pneumoconiosis at an increased risk for? Pt with silocosis?
Pt with asbestosis?
Coal miner and Silicosis: TB (not CA)

Silicosis: increased risk for CA (no risk for TB)

What is the cause of silicosis?
Exposure to free silica dust seen in miners, glass manufacturers, stone cutters, sand blasters.

What does a lung from a pt with silicosis look like?
Nodular, with fibrotic masses that are filled with silica crystals

How does a nonsmoker that was a roofer 20yrs ago differ from a smoker?
If both were exposed to asbestos by their roof work:

Smoker + asbestosis = bronchogenic carcinoma (any primary lung CA) over malignant mesothelioma

Nonsmoker + asbestos = malignant mesotheloma (takes 25yrs to develop)

What does a lung from a pt with asbestos look like?
Asbestos: fibrocalcific plaques on parietal pleura and can see asbestos bodies (ferruginous bodies) which are asbestos fibers covered in iron and proteins.

Sarcoidosis (guaranteed on test): describe the 9 characteristic findings
Sarcoidosis (unknown etiology/more common in african lineage)
1. noncaseating granulomas involving many organ systems
2. huge hilar lymphnodes
3. uveitis (blurred vision - in back of eye!)
4. hypercalcemia (macrophages make 1-alpha hydroxylase, hydroxilating VitD = increased VitD!
5. increased ACE
6. low CD4 Th (used up in making granuloma
7. salivary gland enlargment
8. reduced sensitivty to skin tests (neg TB)
9. erythema nodosum of skin

What causes granulomas in lungs (3)
1. TB
2. Histoplasmosis
3. Sarcoidosis

Rx for sarcoidosis?

Where do most pulmonary emboli originate from?
Femoral vein - most common site of embolization (veins in legs are most common site of thrombosis)

How do you screen for pulmonary emboli?
Ventilation/perfusion scan

Does a saddle embolus cause an infarction?
No, not enough time to infarct - sudden death from blocking pulmonary artery

Two types of pulmonary edemas?
1. increased hydrostatic pressure: as a result of left ventricular failure or mitral stenosis

2. increased alveolary capillary permeability: in infections/inflammatory rxns/drug OD

Four main causes of pulmonary hypertension?
1. chronic hypoxemia: hypoxemia vasoconstricts pulmonary vessels and vasodilates peripheral vessels

2. loss of pulmonary vasculature (COPD)

3. left to right shunts (right heart failure)

4. mitral stenosis with back up of blood flow in the pulmonary veins.

Cor pulmonale
Pulmonary HT that leads to right ventricular hypertrophy

Compare atypical pneumo presenation to typical?
Atypical: no productive cough or very high temp (they are interstitial; inflam of intersitium so there is no exudate in alveoli - no consolidation)
slow and incideous onset
MCC: Mycoplasma pneumo, 2nd: Chlamydia
3rd: legionella

sudden 103 fever
feel horrible
hurting big time
productive cough (have exudate and consolidation - pus in alveoli)
MCC: Strep Pneumo

What is mycoplasma pneumonia associated with?
Cold agglutins

What is the MCC of spontaneous pneumothorax?
A ruptured subpleural bleb (common in tall men that can get these in there apex as well as scuba divers)

What is a pneumothorax? how is it formed?
Beneath pleura a air pocket forms --> can rupture --> causes a hole in the pleura --> collapses lung becuase of neg intrathoracic pressure is what keeps lungs expanded.

What happens to the diaphragm and the trachea in a spont pneumothorax?
Diaphragm will go up on that side and trachea will GO TO COLLAPSED side (there is space!)

Describe a tension pneumothorax:
Completely different from spont: MCC knife injury

Tear of pleura that is a flap --> breathe in and flap goes up and air goes into pleural cavity. Expiration --> flap closes and air stays in cavity --> increase in pressure --> pushes trachea and lung to the other side and you get compression and atalectasis (diaphragm will be pushed down; compression can involve the vena cava and right ventricle --> decrease blood return --> medical emergency)

4 problems in CF patients associated with P.Aeruginosa?
1. pneumonia
2. bronchiectasis
3. sepsis
4. tension pneumothorax from ruptured pneumatocytes

Cave explorer in Arizona with resp infection?
Coccidomycosis (not histo; too dry a climate and mainly in Ohio and Midwest)

Bridge painter in NYC with respiratory infection?
Most likely histo (starling dung) or crypto (pigeons)

Rx: amphotercin

Six diseases where Strept Pneumo is MCC?
1. community acquired pneumo
2. meningitis in adults > 18
3. otitis media
4. spontaneous peritonitis in children with ascites
5. sepsis in children with HbSS
6. sinusitis

Seven diseases where P. Aeurginosa is MCC?
1. ICU pneumonia
2. COD in burn patients
3. COD in cystic fibrosis
4. cellulitis/osteomyelitis in puncture wounds of foot in patients with rubber footwear
5. malignant external otitis in diabetes
6. ecthyma gangrenosum
7. hot tube follicultis

Elderly man who lives at home with his wife develops pneumo: Dx?
Strept pneumo

Two potential causes of CXR postive for RML pneumonia (obscures right margin of the heart)
1. bronchogenic CA
2. aspiration with the patient lying down

Afebrile infant with staccato cough, signs of hyperaeration, conjunctivits?
Chlamydia Trachomatis pneumo

What can you see on a chest xr of a pt with a lung abscess
A air/fluid level (cavity is fluid filled with foul smelling sputum)

What is the gold standard in diagnosing a pulmonary embolus?
Pulmonary angiogram

USMLE: Gross photo of a large saddle emboli in a patient on prolonged bed rest? what exactly did this pt die of?
Acute right heart strain

USMLE: What is deficient in Kartagner's syndrome? Describe morphological findings:
Kartagner's: absent dynein arm in cilia

Situs inversus: but vessels and chambers in the heart are still normal

Infertility in males/females
Sinus infections

Describe the inital infection findings in primary tuberculosis?
Primary infection is characterized by a Ghon complex: TB granulomas in a lung lobe (usually lower) AND perihilar lymph nodes.

Describe the findings in reactivation TB?
Cavitary lesion (often in upper lobe) that is described in first aid as "fibrocaseous".

Extrapulmonary tuberulosis can develop in CNS, vertebral body, lymphadenitis, KIDNEY, and GI.

What do these three other type of mycobacterium cause:

M.Kansasii: pulmonary TB-like symptoms
M.Scrofulaceum: cervical lymphadenitis in kids
M.Avium: intracellular, often resistant to multiple drugs; causes disseminated disease in AIDS (mycobacterium avium complex)

All mycobacterium are acid-fast

Describe characterisitics of Mycobacterium Leprae?
acid fast
likes cool temperatures
infects skin and superficial nerves
cannot be grown in vitro
reservoir: armadillos
Rx: dapsone (tox is hemolysis and methemoglobininemia)
Alternative treatment: rifampin and combo of clofazimine and dapsone.

What are the two forms of Hansen's disease?
1. Lepromatous: failed cell-mediated immunity (LEpromatous is LEthal)

2. Tuberculoid: self-limited

In TB, which stage is a cavitation associated with?
Secondary TB

Pt comes in with cavitary lesion in upper lobes: DDX? (4)
Great test to use to get Dx?
Squamous cell CA
Klebsiella pneumo (thick mucoid wall)

Test: do an acid-fast stain to stain for mycolic acid (thick lipid layer of mycobacterium TB would stain acid fast)

Describe miliary spread of TB:
Miliary spread: when TB spreads via lymphatics and blood (hematogenous) --> causes miliary spread in which seeding of distal organs with innumerable small millet seed-like lesions

Is a positive TB skin test possible in primary TB as well as secondary?

Two things associated with atelectasis in neonates?
1. prematurity
2. intrauterine fetal anoxia

What is a chylous effusion?
Lymphatic fluid from large tumor damaging thoracic duct allowing chylomicron rich lymphatic fluid from the abdomen to drain into the pleural cavity rather than the vena cava.

Describe transudate and when it occurs?
Transudate: low protein content; due to CHF, nephrotic syndrome, or hepatic cirrhosis.

Describe exudate and when it occures?
Exudate: high protein content, cloudy.
Can be caused by malignancy, pneumonia, collagen vascular dz, trauma, and INFECTIONS

How does the finding of tactile fremitus differ in bronchial obstruction, pleural effusion, and lobar pneumonia?
Bronchial obstruction and pleural effusion: decreased tactile fremitus (loss of aeration)

Pneumo: increased fremitus
What is the 2nd MCC of CA in men and women?
What is the MCC of death due to CA in men and women?

How is the incidence of lung cancer changing in men and women?
Decreasing in men and increasing in women

Three MC primary lung CA in descending order:
1. AdenoCA: MC in nonsmokers
Located peripherally
Clara cells --> type II pneumocytes
Multiple densities on CXR

2. Squamous cell CA: ectopically secrete PTH-like peptide (hypercalcemia)
Hilar mass arising from bronchus
Keratin pearls and intercellular bridges

3. Small cell CA: ectopically secrete ACTH (ectopic Cushings) and ADH (SiADH)
Most malignant
May lead to Lambert-Eaton syndrome
Neoplasm of neuroendocrine Kulchitsky cells (small darkblue)

What is a Pancoast tumor?
Carcinoma of the apex of the lung that may affect cervical sympathetic plexus, causing Horner's syndrome
Usually located in the posterior mediastinum and often caused by squamous CA

AKA: superior sulcus tumor

What is the cause of nasopharyngeal CA and where in the world is it most commonly seen?
Cause EPV virus

What is the most common CA OF THE LUNG?
METASTASIS!!! Breast is the most common metastases.

Brain, bone, and liver are also common.

What is a carcinoid tumor?
A low grade malignancy that secretes serotonin and can causes carcinoid syndrome (flushing, diarrhea, wheezing, and salivation)

(very uncommon)

Describe a large cell lung CA:
Peripherally located
Highly anaplastic undifferentiated tumor
poor prognosis
No relationship to smoking
Pleomorphic giant cells with leukocyte fragments in cytoplasm

Does tumor stage or grade consider histological features of the tumor?

What are the six complications of lung CA?
Superior vena cava syndrome
Endocrine (paraneoplastic)
Recurrent laryngeal symptoms
Effusions (pleural or pericardial)

Why will you never a get an enteritis from rhino virus?
because it is destroyed in teh stomach (acid liable)

Is there a vaccine for rhinovirus?
No, and there will never be! 100+ serotypes

What is superior vena cava syndrome?
Compression or invasion of the superior vena cava resulting in facial swelling and cyanosis along with dilation of the veins of the head, neck, and upper extremities.

Note: this one just blocks off superior vena cava; don't confuse with Pancoast

What findings, other than Horner's syndrome can you find in a Pancoast tumor?
Brachial plexus findings since it is involved in the apex of the lung