UW Step 2 im mostly pulmonary

tinnitus, nasuea/vomiting and fever, AMS, acid base abnormalities in OD

Salicylate intox. Tx includes alkalinization of the urine with sodium bicarb.

AE: Increased airway resistance, bradycardia, fatigue and depression

beta blockers

Aspiration pna treatment

clindamycin- patients who had recent stroke, hx of unconsciousness (heavy alcohol user), recent sedation for procedures (endoscopy, etc), etc

Elevated bp and heart rate, feeligns of euphoria, increased alertness. Cardiac ischemia, intracranial hemorrhage in od

cocaine intox

Headache, vomiting, abd pain, flushed skin, on od

cyanide toxicity. Inhalation exposure causes a bitter almond odor

organism endemic in the MIssissippi and ohio river valleys and central america

histoplasma capsulatum- dimorphic fungus. common and usually asymptomatic infection. Usually found in soil with a high concentration of bird or bat guano droppings. Infection is contracted by inhalation fo the spores or mycelial fragments. Infection is very common in endemic areas and most pp are infected before adulthood. Less than 5% of pp develop the symptomatic disease. Extent of disease is determined by amt of exposure and immunity of the host. Symptomatic lung infection is most commonly caharacterized by self-limiting fever, chills, nonproductive cough. CXR may show patchy lobar or multinodular lobar infiltrates. Chronic cavitary pulmonary histo is a progressive, fatal form of histoplasmosis that usually develops in older COPD patients. disseminated histo is seen in immunocompromised adults and young children.

60/M hx of HTN and CAD > emergency laparotomy for a perforated peptic ulcer. Sustained an MI 5 years ago, currently treated with a beta blocker. REceives 4L of IV normal saline intraoperatively. S/P sx, patient extubated, develops mild respiratory distress. ABG on room air: Bicarb 22meq/L pH 7.46 PaO2 55 PaCO2 33 Temp BP nml, pulse 110 regular. Lungs bilateral crackles at lower lung fields.

hypoxic patient likely has pumonary edema due to acute decompensated heart failure. Causes can be classified into reduced inspired O2 tension, hypoventilation, shunt, V/Q mismatch and diffusion limitation. A-a gradient estimates teh degree of alveolar o2 transfer to the blood. This pt's alveolar oxygen is calculated using the following equation: PAO2 = (FiO2 x [Patm-PH2O]) - (PaCO2/R) PAO2 = 149.73 - PaCO2/0.8> plug in 33 in this case for a total of 108.5 A-a gradient = PAO2-PaO2 = 108.5-55 = 53.5 Elevated A-a gradient is due to diffusion limitation (eg interstitial diseases), V/Q mismatch (eg, pulmonary edema), or shunt (eg, intracardiac shunts). V/Q mismatch refers to an imbalance of blood flow and ventilation. When ventilation is obstructed and blood flow is unchanged (as in emphysema), there is a decrease in O2 and an increase in CO2. When blood flow is excessive relative to ventilation, (eg pulmonary edema, pneumonia, atelectasis), there's a decrease in O2. Pt's hx of cad with sudden dyspnea after IV fluids makes V/Q mismatch due to pulmonary edema more likely than a shunt. The excess fluid reduces lung compliance by preventing some alveoli from fulling exapnding. Supplemental O2 usually corrects the hypxemia, V/Q mismatch and A-a gradient.

Tx of moderate persistent asthma

in addition to a prn albuterol inhaler and a low-dose inhaled corticosteroid, pts with moderate persistent asthma (daily sx, weekly nighttime awakenings, and FEV1 60-80% of predicted) should be prescribed a long-acting inhaled beta-2 agonist inhaler.

AIDS patients and progressive multifocal leukoencephalopathy in AIDS patients

is a demyelinating disease that can occur in patients with HIV/AIDS, but is less likely in patients on HAART and usually occurs only in patients with CD4 counts < 200/mm3. In addition, hearing loss would be an atypical presenting sx in patients with PML.

rinne left neg, weber normal

left conductive

rinne neg on left, weber lat to left

left conductive hearing loss

rinne left neg, weber lat to right

left mixed hearing loss

Aphthous stomatitis

localized, shallow, painful ulcers with a gray base. Recurrent is the most common cause of oral ulcers

Thick-walled cavitary lesion son cxr. Cough, hemoptysis, fever and the production of purulent sputum

lung abscess

Serum AFP is a marker for

malignancies such as hepatocellular carcinoma and testicular cancer.

Classic chest xray findings of PCP PNA

may be normal/vary, classic is bilateral interstitial and/or alveolar infiltrates. Sputum induction with hypertonic saline is the first line method of dx b/c it is minimally invasive- though highly specific, only 50% sensitive. When Sputum induction doesn't confirm dx, BAL is performed. For PCP dx, BAL has >90% sensitivity and specificity.

depressed mental status, depressed respiratory rate and effort, small constricted pupils (miosis)

opioid overdose

PE of Pumonary emoblism

presents with acute-onset dyspnea, tachypnea, and pleural chest pain. Patients have hypoxemia and respiratory alkalosis with a widened A-a oxygen gradient

37/F 1 day of dyspnea. complains of right sided chest pain but denies cough and fever. other med problems include a long hx of ms and an episode of afib dx in the ed 2 weeks ago that resolved spontaneously. She is a wheelchair user due to spastic paraparesis and has saccadic speech. She is allergic to penicillin. Her bp is 120/70, pulse 110/min and regular, and respirations are 24/min. Her pulse ox shows 90% at room air. CXR shows right sided pleural effusion. Therapeutic thoracentesis is performed. Her lab results reveal Pleural fluid Glucose 100mg/dl Protein 3.1 g/dl WBC 150 RBC 230 LDH 220 Serum electrolytes Glucose 110 LDH 300 Protein 5.8 Most likely cause of pleural effusion

pulmonary embolism. Pleural fluid protein/serum protein ratio >0.5, LDH ratio >0 .6, and a pleural fluid LDH level greater than 2/3 of the upper limit for normal for serum LDH level. She has an exudative effusion by all 3 criteria. Causes include infection (eg pna and tuberculosis), malignancy, PE, connective tissue disease and iatrogenic causes. This pt who uses a wheelchair most likely has a PE from a DVT in one of he immobilized legs. Over 1/2 the pts with a DVT in a proximal leg vein will experience a PE manifesting clinically with dyspnea, tachypnea and pleuritic chest pain. Arterial blood gas analysis in this setting typically shows resp alk and a widened A-a gradient due to v/q mismatch. CXR can be normal or show evidence of atelectasis and/or pleural effusion. When pleural effusions develop, the pleural fluid can be exudative (more common) or transudative, with varying composition. While pulmonary angiography is the gold standard for diagnosing PE, helical computed tomography scan is the diagnostic test of choice in practice.

cardiomegaly, cephalization of pulmonary vessels with prominent vascular markings, Kerley b lines, pleural effusions

pulmonary venous congestion- CHF.

Treatment of moderate to severe asthma exacerbation

requires SABA, ipratropium nebulizer, and systemic corticosteroids. Adding ipratropium to SABA causes greater bronchodilation than either agent alone. The current guidelines recommend the addition of ipratropium for management of severe exacerbations early in teh course of the disease. Systemic glucocorticoids (oral or intravenous) increase the rate of symptomatic improvement, but their beneficial effects are not clinically apparent for several hours after administration. A one time infusion of intravenous magnesium sulfate is also recommended for severe asthma exacerbation without improvement after 1 hour of therapy or for life-threatening asthma with impending respiratory failure.

Rinne neg on right, weber normal

right conductive

rinne neg on right, weber lat to right

right conductive

rinne neg on right, weber lat to left

right mixed hearing loss

African american woman, painful shin lesions, bilateral hilar adenopathy on xray

sarcoidosis.- a chronic multisystem disorder due to noncaseating granulmatous inflammation deposited into various organs. Typically affects young adults, is 3-4 times more common in african americans, and affects more women than men. Frequently detected incidentally on cxr, but can also present with symptoms such as cough, dyspnea, fever, malaise, and weight loss. Sarcoidosis primarily involves the lungs- CXR classically shows bilat hilar adenopathy and/or reticular opacities. Up to 30% of sarcoidosis patients present intitially with extrathoracic manifestations commonly involving the skin (eg erythema nodosum with painful shin lesions), eyes (uveitis) and musculoskeletal system (eg polyarthralgia). Elevated calcium and ace levels are often seen but are not specific for diagnosis. Definitive dx can be established with mediastinoscopy/bronchoscopy for tissue biopsy. Symptomatic pts are usually treated with corticosteroids.

Treatment of patients with intermittent asthma

short-acting bronchodilator (eg albuertol) PRN.

Aspergillosis on CXR

solid mass surrounded by a radiolucent crescent (crescent sign/monod's sign)

Tx of severe persistent asthma

symptoms throughout the day, frequent nighttime awakenings, extremely limited activity, and FEV1 <60% predicted) should receive a PRN albuterol inhaler, long acting beta 2 agonist inhaler, and high-dose inhaled corticosteroids. Oral prednisone can also be used in cases of severe persistent asthma.

Approach to pleural effusion

1. exudative vs. transudative. Exudate at least 1 of the following: Pleural fluid protein/serum protein ratio >0.5 Pleural fluid lactate dehydrogenase (LDH)/serum LDH ratio >0.6 Pleural fluid LDH > 2/3 of the upper limit of normal for serum LDH If all negative = transudative. 2. complicated vs. uncomplicated vs. empyema. Complicated parapneumonic effusions involve persistent bacterial invasion into the pleural space, which decreases pleural fluid glucose <60 mg/dL (utilized by bacteria) and increases LDH (from lysis of neutrophils). Culture is usually negative and the effusion resolves with abx as bacteria can be cleared easily from the pleural space. Complicated effusions can progress to empyema which is frank pus in the pleural space requiring chest tube drainage. This pt's pH of 6.9 and low pleural fluid glucose are more consistent with complicated parapneumonic effusion.

44/M, MVA, placed on mecahnical ventilation. O2 sat repeatedly drops below 90%, requiring gradual increases in the FiO2. On day 3, cxr shows bilateral fluffy infiltrates. No prior med problems and doesn't take any meds. dyspnea, tachypnea, hypoxemia, with bilateral alveolar infiltrates on chest x ray. Labs: Hb 10.1 Plt 160 leukocyte 13,500 Sputum cultures are neg, vent settings are FiO2 90% Tidal volume 400ml Resp rate 12 PEEP 5cm H2o

Acute respiratory distress syndrome. a condition that can develop in the setting of sepsis, severe bleeding, severe infection, toxic ingestions, or burns. In terms of pathophysiology, ARDS develops when inflammatory mediators, released secondary to local or distant tissue injury, damage the alveoli. The resultant increased alveolar capillary permeability allows fluid to leak into the alveoli, causing pulmonary edema. Mechanical ventilation with low tidal volumes and positive end expiratory pressure (PEEP) as a mainstay of therapy. PEEP improves oxygenation by preventing alveolar collapse at the end of expiration, which increases the functional residual capacity and decreases the work of breathing. This patient's PEEP is currently 5cm H2O but in ARDS, levels of up to 15 may be necessary. Increasing this patient's PEEP would be the best way to improve his oxygenation. IN ards, mecahnical ventilation with low tidal volumes and PEEP can improve oxygenation. Potential complications of PEEP include barotrauma and tension pneumothorax.

Patient on mechanical ventilation with an FiO2 of 70%, tidal volume of 370ml and resp rate of 14. ABG: ph 7.45 pO2 59 PCO2 30 HCO3 21 What is hte best next step in managing the patient

Add positive end-expiratory pressure Generally speaking, oxygenation may be improved by further increasing the FiO2 or by adding positive end-expiratory pressure

Persistent nasal blockage, episodes of bronchoconstriction

Aspirin sensitivity syndrome- pseudo-allergic reaction: exaggerated release of vasoactive and inflammatory mediators in susceptible individuals. ASA is a COX1 and COX 2 inhibitor. As the result of its pharmacologic action, arachidonate diverges from blocked COXs to a 5-lipoxygenase pathway. Accumulation of leukotrienes and changed PE/LK balance triggers characteristic reactions (bronchoconstriction/polyp formation) in susceptible individuals. LK inhibitors are gaining popularity in the tx of this condition. Other commonly used tx modalities include topical corticosteroids and aSA desensitization therapy. *****VERY HIGH YIELD question****

Asthma vs. COPD

Asthma and COPD are inflammatory diseases of the resp tract characterized by cough and dyspnea. In general terms, asthma is an atopic disease with a predominantly genetic etiology and early onset of symptoms. COPD is due primarily to smoking and presents later in life. In clinical practice, however, there is significant overlap between these conditions in age of onset, clinical manifestations, and pathophysiologic mechanisms. Differentiating between the 2 is therapeutically relevant as inhaled corticosteroids are the primary long-term intervention for asthma and a long-acting anticholinergic inhaler is generally preferred for COPD. Most efficient test to differentiate asthma and COPD is spirometry before and after administration of a bronchodilator (usually albuterol). Patients with asthma should show significant reversal (>12% increase in forced expiratory volume in 1 second) in airway obstruction after administration of the bronchodilator. Patients with COPD may have partial reversibility with bronchodilators, but restoration of normal airflow after administration of a bronchodilator effectively rules out COPD.

47/M returned from cruise to bahamas, presents with high grade fever, productive cough and SOB for the past 2 days. He also complains of frequent vomiting and diarrhea. He has no prior med problems, doesn't take any meds, and denies using tobacco, alcohol or drugs. Temp 104, bp 110/65, pulse 80, resp 18. Lung exam reveals right lower lobe crackles. Abdomen soft and nontender. CXR demonstrates right lower lobe consolidation. Sputum gram stain contains many neutrophils with no orgs. What antibiotic

Azithromycin Legionella accounts for approx 2-10% of all CAP. Travel-associated legionnaire's disease is a well documented phenomenon that has been linked to cruise ship and hotel water supplies. Sx that help distinguish legionella from other causes of CAP include high grade fever, GI sx, and neurologic sx. Lung exam typically reveals rales and chest radiograph most often reveals focal lobar consolidation. Legionella pneumophila is a gram neg rod that stains poorly because it is primarily intracellular. Therefore sputum gram stain showing many neutrophils but no orgs is also characteristic. Definitive dx may be made by culturing the bac on charcoal agar and/or urinary antigen testing. Legionnaire's disease is treated with either macrolides (azithromycin) or newer generation fluoroquinolones (levofloxacin).

32/F brought to ED by husband for slurred speech and difficulty walking. Has been very drowsy for past several hours. Non-typical behavior. Hx of bipolar disorder, insomnia, migraine headaches, seizures and hypothyroidism. Temp 98.6, bp 110/70, pulse 76, resp 16. She is lethargic and falls asleep during the interview and pe. Pupils are 5mm in size and reactive to light. Neck is supple. Oropharynx is clear. Chest auscultation is unremarkable. Abdomen is soft and nontender. bowel sounds are normal. Limited neurologic exam shows 1+ deep tendon reflexes in all 4 extremities. There's no babinski sign, strength is 5/5 throughout. There is no nystagmus or hand tremor. Blood sugar is 130 mg/dL, which of the following is the most likely cause of her sx?

Benzodiazepine overdose. Pt will present with slurred speech, unsteady gait, and drowsiness. Benzos are used for the tx of anxiety, insomnia, seizures and alcohol withdrawal. During benzo intox, pupil size tends to be normal, with only mild resp depression. Benzo OD can be distinguished from opioid od by the lack of severe resp depression and the lack of pupillary constriction. Furthermore while alcohol and phenytoin intox also share similarities with benzo overdose, they can be distinguished by the presence of nystagmus.

53/M progressively worsening dyspnea over 4mo period. Decreased appetite, weight loss and nagging epigastric discomfort. His pmh significant for a chronic duodenal ulcer for which he takes ranitidine on and off. HE doesn't use tobacco, alcohol or illicit drugs. He has worked as a plumber for the past 30 yrs. On PE, his temp is nml, bp 140/86, pulse 80, resp 15. PE reveals fingernail clubbing and bibasilar end-inspiratory crackles on lung auscultation. CXR demonstrates ground glass opacities of the lower lung fields, multiple pleural plaques and one 3x3 cm mass in the right lung periphery. CT guided biopsy of the mass is planned. Biopsy is most likely to show which of the following?

Bronchogenic carcinoma. Individuals with an occupational hx involving mining, shipbuilding, insulation, or pipe work are at risk for asbestosis. Sx tend to develop 20-30 years after the initial exposure. The most common clinical presentation is dyspnea without cough or sputum production. Bibasilar end inspiratory crackles and clubbing are seen in approx 40-50% of patients with advanced disease. CXR often reveals interstitial abnormalities of the lower lung fields consistent with pulmonary fibrosis. Pleural plaques are also seen in approx 50% of asbestosis CXRs adn help distinguish this condition from other causes of pulmonary fibrosis. In addition to pulmonary fibrosis and pleural plaques, asbestosis in patients are also at increased risk for dev'p certain malignancies. Increases risk of lung cancer 5 fold. Most common malignancy in asbestosis patients is bronchogenic carcinoma.

Conditions that result in clubbing

COPD does NOT cause clubbing. Pulmonary hypertension and hypoxemia due to congenital heart disease often result in clubbing. Also, lung abscesses, bronchiectasis, cystic fibrosis, interstitial lung disease and sarcoidosis. However, the pulmonary htn and hypoxemia of COPD are RARELY associated with digital clubbing. New clubbing in pts with COPD often indicates the development of lung cancer.

64/M SOB, sx 1 week ago with dry caugh and mild fever. PMH htn and exertional angina. Hospitalized 6 mos ago with PNA. 35 pack year smoking hx. BP 140/90, hr 90 and reg. Mild resp distress on PE, uses some accessory resp muscles for breathing but can speak in full sentences. Chest ausc reveals bilat wheezes and crackles at left lung base. ABG: pH 7.36 pO2 72 pCO2 51 Most likely cause

COPD exacerbation characterized by an acute worsening of sx in a pt with chronic lung disease. COPD exacerbation is a very common cause of hospitalization in the US. Upper airway infections (bacterial or viral) are the most common precipitants of COPD exacerbations; such an infection explains the pt's week-long hx of fever and cough. Pts often present with cough and sob, a significant smoking hx is common. Finding bilat wheezes on exam , resp distress, accessory resp muscle use and prolonged expiratory time favors a dx of obstructive lung disease. Finally, the pt's abg shows hypoxia, hypercapnia and resp acidosis. An abg profile consistent with COPD

Causes of conductive hearing loss

Cerumen impaction, middle ear fluid or infection, decreased mvt of the small bones of the ear, bony tumors of the middle ear. Otosclerosis is a common cause of conductive hearing loss in adults, esp patients in their 20s/30s, invovles abnormal remodeling of the otic capsule thought to be a possivle autoimmune process in genetically susceptible individuals. Stapes footplate becomes fixed to teh oval window, resulting in loss of its piston action. Disorder is sometimes referred to as otospongiosis b/c CT scan may show a lucent (as opposed to sclerotic) focus in the temporal bone near the oval window. Tx involves either hearing amplification or surgical stapedectomy.

24/F recurrent painful ulcers in her mouth and occasional abd pain. Unintentional weight loss x 6mos. Biopsy of ulcer shows granulomatous inflammation. Hematocrit is 42%.

Chron's disease- can invove any component of the GI system from mouth to anus, and characteristically has skip lesions. Aphthous ulcers are occasional component of the disease and can be confirmed either with an abdominal CT, a small bowel fluoroscopic study, or endoscopy. Granulomas can be seen pathologically in up to 30% of patients with Crohn's disease, and can confirm the dx in the absence of granulomatous infections. Since pts with this condition often have a nonspecific presentation with weight loss and vague abdominal pain, correlating the pt's sx with any extraintestinal findings asso with Crohn's disease can help to suggest the dx. Celiac would cause weight loss, abd pain and oral ulcers, but no granulomatous inflammation. Folic acid deficiency can cause oral ulcers but not cause abd pain.

60/M c/o cough and dyspneal on exertion. Has had the cough for over 2 yrs but it has gotten worse recently along with increasing sob. No hemoptysis, chest pain or leg swelling. Pt has a 60 pack year smoking hx and drinks 2 ounces of etoh per day. Worked in a shipyard for 10 years. Temp 99, bp 140/80, pulse 80, resp 20/min. CXR shows prominent bronchovascular markings and mild diaphragmatic flattening. Pulmonary fxn test results: Forced expiratory vol in 1 sec 67% of predicted Forced vital capacity 95% of predicted FEV1/FVC ratio 0.65 CO diffusion capacity is 100% of predicted value. Which of the following is the most likely cause of this patient's symptoms

Chronic bronchitis The patient's pulmonary function test findings (decreased forced expiratory vol in 1 sec <70% of predicted, forced vital capacity FVC >80% and decreased FEV1/FVC ratio are consistent with obstructive lund isease. DLCO measures the lung's ability to transfer gas to the blood. CO uptake is influenced by the diffusion capacity of the alveolar cap membrane and the binding of CO and hemoglobin. This pt's normal DLCO indicates intact alveolar and capillary structure. Pt's chronic smoking >1 pack/day for at least 20 yrs, productive cough, dyspnea on exertion, and decreased FEV1/FVC ratio suggest chronic obstructive pulmonary disease. COPD is a group of chronic disorders causing progressive airflow limitation (decreased maximal expiratory flow rate during forced expiration) due to chronic inflammation in the lungs. The main subtypes of COPD include predominant emphysema or chronic bronchitis. Patients with predominant emphysema are genearlly thin with severe dyspnea, hyperinflated chest, decreased vascular markings, decreased DLCO (due to alveolar destruction), and moderate o2 desat. Pts with predominant chronic bronchitis have chronic productive cough x >3 mos x 2 consecutive years not due to other causes (eg bronchiectasis). Chronic bronchitis is due to hypersecretion of mucus and structural changes in teh tracheobronchial tree after prolonged exposure to nonspecific irritants. It usually presents with prominent bronchovascular markings, mildly flattened diaphragm and normal DLCO.

Good gram negative coverage but isn't effective for anaerobic or most gram positive organisms

Ciprofloxacin

36/F fever and productive cough. Suspected CAP and prescribed Azithromycin x 5d. After 5d, no improvement and complains of worsening foul smelling sputum. Had upper GI endoscopy 8 days prior for long hx of heartburn and suspected peptic ulcer disease. Also reports a hx of manic-type bipolar disorder. BP 130/80, her pulse 108/min, temp 101.6, resp 26, CXR showed right upper lobe infiltrate. Which therapy would be most helpful for this patient's condition?

Clindamycin This patient likely has an anaerobic pneumonia as a complication of upper GI endoscopy (aspiration pna). Patients with PNA caused by anaerobic organisms typically present with systemic sx such as fever and malaise as well as a characteristic foul-smelling sputum. Patients with poor dentition, who have a greater quantity of anaerobic organisms in their mouth, are at greater risk of anaerobic aspiration pna. The location of the infiltrate depends on the patient's body position when the aspiration occurs as the infectious agents tend to settle in dependent lung zones, such as the poasterior segments of the upper lobes (recumbent) and the superior and basilar segments of the lower lobes (standing). Adding an antibiotic with anaerobic coverage such as clindamycin is the most reasonable next step.

38/F recent episode of hemoptysis. Sx started 5 days ago with malaise, throat pain and dry cough. Cough progressed becoming productive of yellowish sputum. She started noticing speckles of red blood in her sputum as of yesterday. Her pmh is significant for peptic ulcer disease. She has no smoking hx. Her temp is 98. BP is 132/81 and HR 87. PE reveals scattered bilateral wheezes. CXR shows clear lung fields. Appropriate next step in mgmt?

Close observation and supportive care. The pt described is a young female with no smoking hx presenting with an acute-onset cough productive of yellow, blood-tinged sputum. The most likely cause of hemoptysis in this case is acute bronchitis; an exacerbation of chronic bronchitis is lesslikely though possible. This dx is supported by a lack of historical or physical exam evidence for more serious conditions as well as by the patient's accompanying malaise and throat pain. Additionally, fever is uncommon in acute bronchitis. But wheezing is a common PE finding in this dx. The presence of fever would suggest a more severe dx such as pna while constitutional signs, weight loss or more significant hemoptysis may suggest malignancy or tuberculosis. Acute bronchitis is most commonly viral in etiology, so antibiotics are not indicated. In these cases, observation and close follow-up is the most appropriate treatment strategy.

67/smoker presents to ED with 3day hx of sob and cough. PMH sig for tuberculosis 10 years ago, tx with 6 mos of multidrug reg. Also has a hx of hypertension and takes amlodipine. On exam, bp 140/90 adn hr 110. Breath sounds over right lover lung area have full inspiratory and expiratory phases. Over teh same area, there's dullness to percussion and increased fremitus. Pt also has trace ankle edema. What accounts for all of these findings?

Consolidation. This pt has sx and PE findings consistent with lobar CAP. CAP usually presents with fever, chills, cough, purulent sputum and chest pain, plus evidence of alveolar consolidation (bronchial breath sounds, dullness to percussion, increased tactile fremitus, egophony, whispered pectoriloquy, and bronchophony on PE). Note- elderly pts with pna may not have fever or elevated white blood cell count. The patients trace edema could be from amlodipine.

43/M hospitalized for acute pancreatitis. On day 3 he develops respiratory distress. Tx to ICU and intubated. FiO2 0.8 RR 14 Tidal Volume 380 PEEP 7mm H2o 10 minutes after intubated, bp 110/70, hr 90/min and abg are pH 7.42 pO2 105 PCO2 37 Best next step in management

Decrease FiO2 Acute pancreatitis causes ARDS in approx 15% of pts. Mechanical ventilation improves oxygenation by providing an increased fraction of inspired oxygen (FiO2 and by providing PEEP to prevent alveolar collapse. In the hospital setting, the arterial pO2 provides an important measure of oxygenation. It is influenced mainly by the FiO2 and the PEEP level. The arterial pCO2, a measure of ventilation, is affected mainly by the respiratory rate adn tidal volume. Normal FiO2 at sea level is 21%. Pts are often provided a high FiO2 (>80%) initially, pending the results of the first ABG. The ventilator settings can subsequently be adjusted based on these results. The goal is to maintain paO2 > 60). An important early goal in initial ventilator managment should be to decrease the FiO2 to non-toxic values. There is no strict cut-off FiO2 value for O2 tox, but levels below 50-60% are desirable. In this case, teh pt's initial abg values indicate appropriate ventilation adn excessive oxygenation, thus FiO2 should be slowly decreased to below 60% to prevent oxygen tox to the lungs.

Bronchiectasis on a CT?

Dialted central bronchi which are larger than the adjacent pulmonary artery branches as well as thickening of the bronchial walls, which is consistent with bronchiectasis. Pts with bronchiectasis generally present with chronic productive cough and are often treated with repeated courses of abx. The presentation can be similar to COPD, as the abnormal airways cause obstructive signs and sx. Hemoptysis, sometimes massive to the pt of requiring bronchial artery embolization is a potential complication that can occur in some pts. CT is the best method to confirm the diagnosis in patients with a suggestive presentation.

59/M brought to ed b/c of severe dyspnea and left sided chest discomfort. He was driving to work when he suddenly began to feel weak and sob. His other med problems include a long hx of COPD, esophageal reflux and chronic pyelonephritis. He has smoked one pack of cigs daily x 35 years. His current meds include ranitidine, inhaled ipratropium, and albuterol as needed. PE reveals trace ankle edema, markedly decreased breath sounds over the left chest, and scattered wheezes over the right chest. An EKG shows sinus tachycardia. ABG reveals pH 7.42 PaO2 59 PaCO2 41mm Hg Which is the underlying mechanism of the patient's current disorder

Dilated apical alveoli (blebs) The patient presents with signs/sx of spontaneous pneumothorax which is commonly caused by COPD. Cig smoking markedly increases the risk of a pneumothorax and it is thought that smoking leads to chronic airway inflammation and a form of resp bronchiolitis. The chronic obstruction of alveolar sacs leads to the formation of large alveolar blebs (generally in the upper lobes), which can eventually rupture and leak air into the pleural space. Patients with pneumothorax typically present with acute onset of chest pain and sob. ON the affected side, breath sounds are markedly reduced and the chest is hyperresonant to percussion. In a patient with COPD presenting with catastrophic worsening of their resp sx, spontaneous secondary pneumothorax should always be suspected.

29/M brought to the ED due to sudden onset confusino and fever. Recently admitted for hallucinations and d/c in stable condition. Temp 101.6. BP 150/100, pulse 112. Resp 24. Mucus membranes are dry, profuse diaphoresis is present. Lungs are clear to auscultation, ab muscles are rigid. Muscle tone is increased; lead pipe rigidity is noted in all 4 extremities. DTR are 2+, tremor is noted. Most likely diagnosis?

Drug induced idiosyncratic reaction The combination of recent onset confusion, fever, muscle rigidity and diaphoresis are consistent with the diagnosis of neuroleptic malignant syndrome, a drug induced idiosyncratic reaction. This patient was recently admitted for hallucinations and was likely discharged on a dopaminergic antagonist medication, such as haloperidol. The 'typical' neuroleptic agents (such as haldol) are most frequently implicated in NMS but other dopaminergic antagonists including the 'atypicals' have also been implicated. Symptoms of NMS begin within 2 weeks of initiation of the precipitating drug and mortality rates range from 10-20%. The rigidity and hyperthermia of NMS may result in muscle necrosis, reflected by elevated creatine kinase. Leukocytosis and electrolyte abnormalities are also common. Immediate cessation of the causative agent is recommended.

Unilateral exudative pleural effusion along with pleural fluid pH < 7.2, glucose <60mg/dL or pleural fluid/serum glucose ratio <0.5.

Drug induced lupus can cause this. Hydralazine, procainamide, isoniazid, etc can cause this. Other causes include rheumatoid pleurisy, tuberculosis and malignancy.

Treatment of COPD

Due to cigarette smoking (typically), COPD causes gradually decreasing expiratory flow rates, increased lung compliance, and increased lung volumes. THe only therapies proven to provlong survival in patients with COPD are smoking cessation, supplemental oxygen, and lung reduction sx in certain patients. The remainder of therapies are aimed at decreasing respiratory symptoms, improving quality of life, and decreasing hospitalizations. The mainstays of tx are inhaled bronchodilaters, especially anti-cholinergic meds like ipratropium and tiotropium. Anti-M agents may be combined with short-acting beta agonists like albuterol. Inhaled steroids and long acting beta agonists may be used for patients with more severe COPD

60/m found in the street one winter morning. Had been taking Ibu for headaches, fluphenazine for his schizophrenia and amitriptyline for chronic painful neuropathy secondary to postherpetic neuralgia. He is also receiving cephalexin for for cellulitis of the right lower leg. His temp is 90, bp 80/50, pulse 88, resp 12. Which med most likely contributed to the development of hypothermia in this pt?

Fluphenazine is a 'typical' aps that is commonly injected every 2-3 weeks in schizophrenics with poor compliance. More potent than haldol, fluphenazine can cause hypothermia by inhibiting the body's shivering mechanism and/or inhibiting autonomic thermoregulation. For this reason, pts taking aps meds should be advised to avoid prolonged exposure to cold temps. Under such conditions, they cna develop extreme hyperthermia.

40/M presents to the ED with SOB, cough, hemoptysis for the past 2 days. Says he's never had sx like these before. PMH significant for a non-healing leg ulcer and chronic purulent nasal discharge. He has smoked a pack of cigarettes daily for the past 20 years. On PE, his temp is 99.7, bp is 130/90, pulse 94/min, rr 18/min. Lung auscultation reveals patchy rales bilaterally. Heart sounds are regular. 2x3 cm ulcer with rolled, undetermined borders is noted on teh right lower leg. Best explanation for hemoptysis?

Granulomatosis with polyangiitis (Wegener's) defined clinically as the triad of systemic vasculitis, upper and lower airway granulomatous inflammation and glomerulonephritis. Disease onset is usually around age 40, with men and women equally affected. The upper resp tract is the most common site of involvement and sx presentation. Granulomatous inflammation in the nasopharynx causes epistaxis, purulent rhinorrhea, otitis, sinusitis, and over time, saddle nose deformity due to the destruction of the nasal cartilage. Cutaneous manifestations are varied and include painful subcutaneous nodules, palpable purpura and/or pyoderma gangrenosum-like lesions as in the patient described above. Lab testing typically demonstrates a positive C-ANCA due to antibodies against proteinase-3 and an elevated CRP. Urinarlysis shows RBC casts, proteinuria and sterile pyuria if glomerulonephritis is present. Treatment is with cytotoxic agents such as cyclophosphamide.

24/M brought to ED with acute asthma exacerbation. Current meds include inhaled fluticasone and salmeterol. Attack started 10 hrs ago, didn't respond to numerous albuterol inhalations and systemic steroids. BP 120/70 and HR is 110. Pt is tachypneic and speaks with difficulty. LUng auscultation reveals decreased breath sounds, prolonged expiration and bilat wheezing. Pulse ox showed 86% on room air. ABG at room air are pH 7.43, Po2 68, Pco2-40. CXR demonstrates hyperinflated lungs. Which of the following findings indicates that the patient is getting worse?

In determining the severity of an asthma attack, it is very important in choosing an appropriate management tactic. Normal PCO2 is one of the indicators of a severe attack. During asthma exacerbation, hyperventilation (tachypnea) is usually present, and the work of breathing is increased. PO2 is usually depressed (but 68 is not bad) because of the V/Q mismatch, and tachypnea is usually present. At the same time, PCO2 is decreased due to hyperventilation. Normal to increased PCO2 values indicates CO2 retention because of severe airway obstruction (air trapping) and/or respiratory muscle fatigue. Other indicators of severe attack include speech difficulty, diaphoresis, altered sensorium, cyanosis and 'silent' lungs. Lung hyperinflation and tachycardia are typical findings during an asthma attack are not indicators of severity.

Tremors, ataxia, altered mental status, nausea, vomiting and hypotension

Lithium intoxication

Erythema nodosum, hilar adenopathy, migratory polyarthralgias, fever

Lofgren's syndrome, seen in Sarcoidosis

34/homeless man brought to ED in confused state. Complains of epigastric pain, vomiting and blurred vision. 98.2, bp is 110/60, pulse 110 and rr 22. PE shows poor oral hygiene and dry mucous membranes. Lungs are clear to auscultation. Abdominal exam shows mild epigastric discomfort. Funduscopic exam reveals optic disc hyperemia. Cause of his sx? Serum sodium 136 Serum K 3 Chloride 93 Bicarb 6 BUN 30 Serum cr 0.8 Blood glucose 80 Serum ketones neg plasma lactate 2.2

Methanol poisoning. Within 24 hrs of ingestion, methanol can lead to headache, nausea, vomiting and epigastric pain. Most severe consequences of methanol intox are vision loss and coma. PE in methanol intox shows optic disc hyperemia and lab studies reveal anion gap metabolic acidosis. An increased osmolar gap is often seen as well. In this pt, the anion gap, calculated by the equation: Na-Cl + HCO3 = 136-93+6 = 37. This value is well above the normal anion gap of 8-12. Such profound metabolic acidosis and very low bicarb 6meq/L can be caused by methanol and ethylene glycol poisoning. There are many other causes of anion gap metabolic acidosis but in the setting of blurred vision, epigastric pain, vomiting and hyperemic optic disc, this patient is most likely suffering from methanol poisoning. The patient's hypokalemia is the likely result of alcoholism and vomiting.

38/homeless man to ed- obtunded, unable to speak. No pmh known. Temp 93.2, bp 90/60, pulse 60, resp 6. O2 sat 86% on room air. Pupils 5mm in size bilat. Oropharynx dry. Lungs are clear to auscultation. abd soft, bowel sounds decreased. no organomegaly. Extremities reveal several needle marks. Babinski neg, dtr 2+ throughout. most appropriate next step in management.

Naloxone- overall, this pt's presentation is consistent with opioid intox. Most reliable and predictive sign in opioid intox is a decreased resp rate. In addition, this pt's obtunded state, decreased bowel sounds, hypotension and hypothermia (result of environmental exposure and impaired thermogenesis) are also consistent with opioid intox. furthermore, needle marks on the extremities indicate a hx of heroin inj. the only part of this patient's exam that is not classic for opioid intox is his normal pupillary size, hoever, normal or even enlarged pupils are not uncommon in opioid intox as coingestants can counteract miosis. An important part of tx for this pt is to administer naloxone, with the goal of increasing his rr from 6/min to 12/min or greater and improving his o2 sat.

ACEI: MOA of cough

Nonproductive cough- 5-20% of patients on them. Accumulation of kinins and possible activatino of the arachidonic acid pathway. Kinins are degraded by ACE, therefore they accumulate as a result of ACE inhibitor therapy. Another physiologic effect is an increase in serum renin level, but this isn't responsible for producing cough. Beta adrenoceptor blockers can cause bronchoconstriction and can precipitate an acute attack in asthmatic patients but otherwise, cough is not typical for these agents.

24/F ingested 14 usual strength acetaminophen tabs 2 hrs ago. Denies any sx. Drinks etoh on weekends. alert and oriented. temp 99, bp 110/60, pulse 90, resp 18. Lab: Hct 40%, WBC 6000, Platelet 390,000. Most appropriate next step in management

Obtain serum acetaminophen levels in 2 hours Patients at early stage of APA intox tend to present with nonspecific signs such as nausea, vomiting, and anorexia. In pts who are within 4 hrs of ingestion, administering activated charcoal in order to decrease absorption would be appropriate. However obtaining an APAP level wouldn't help in predicting hepatotox. Rumack-Matthew nomogram provides the likelihood of hepatotoxic effects of APA overdose based on plasma level and hrs since ingestion. First point on curve is 4 hrs. Mucomist is antidote for od and as long as it is administered within 8 hrs of ingestion, the outcome will not be adversely affected. In this patient, the proper course of action would be to administer activated charcoal. Obtain the plasma APAP level at 4 hrs and then decide whether to administer N-acetylcysteine based on result.

agitated, combative behavior, hallucinating, temp 100, bp 160/90, pulse 126, resp 18. Confused and agitated during exam. Pupils 6mm diameter, respond to light, prominent nystagmus is present. Most likely diagnosis?

Pencyclidine- causes hallucinations, dissociative feelings, agitation, confusion, pupillary dilation, tachycardia, nystagmus. Only illicit drug that causes vertical nystagmus, but horizontal and rotatory nystagmus can also occur. In many cases it can lead to psychotic and violent behavior. High doses can cause severe hypertension, seizures, and life-threatening hyperthermia. Benzos are used for tx of severe psychomotor agitation.

68/M hospitalized s/p intracerebral hemorrhage. On hosp day 3, develops redness, swelling, and tenderness of the left calc. No fever. Thrombus in popliteal vein on US. NExt step in management

Placement of an inferior vena cava filter Proximal DVTs require treatment to prevent acute PE. Most patients are treated acutely with heparin, then managed with warfarin over the long term. HOwever, there are absolute contraindications to anticoagulation including recent sx, hemorrhagic stroke, bleeding diathesis, and active bleeding. In pts with contraindications to anticoag, a hx of complications from anticoagulation (Heparin-induced thrombocytopenia) and in pts who develop a DVT or PE despite receiving anticoagulation, the use of an IVC filter is appropriate. IVC filters may be placed via a transvenous approach, and inhibit progression of lower extremity clots through the IVC towards the lungs. IVCf ilters mayb e permanent or removable. While there's debate re long term effectiveness, they have been proven to prevent PE in pts with DVT in the acute setting.

60/F progressive SOB x 1 month. 30 lb weight loss during this period, hx of htn and hypothyroidism, on metoprolol and levo. smoked 2 packs x 35 years. decreased breath sounds and dullness to percussion on the right, middle and lower lobes of lung.

Pleural effusion- first step is to determine the cause of pleural effusion, and mgmt starts with determining transudate vs. exudate. Diagnostic thoracentesis in non-heart failure patients. lung carcinoma, breast carcinoma and lymphoma are the 3 tumors that cause approx 75% of all malignant pleural effusions. **********extremely high yield******

What 3 diseases account for >90% of chronic cough in nonsmokers who do not have pulmonary disease?

Postnasal drip, GERD and asthma Postnasal drip empiric tx includes oral first gen antihistamine or combined antihistamine-decongestant eg brompheniramine + pseudoephedrine

Frequent nose bleeds in pregnancy

Pregnant women have an increased incidence of pyogenic granulomas on the anterior nasal septum. Highly vascular lesions that are frequent sources of nose bleeds during pregnancy.

Pneumothorax PE

Presents with acute-onset pleuritic chest pain and dyspnea when it is symptomatic. Physical examination reveals hyperresonance to percussion, diminished tactile and vocal fremitus, and decreased or absent breath sounds in the affected area.

34/homeless/M to ER in a confused state. Complains of flank pain. PMH unknown. Temp 98.2. BP 110/60, pulse 110, resp 22. Appearance disheveled. Pupils equal, 4mm in size and reactive to light. Fuduscopic examination is within normal limits. Lungs have crackles in both bases. Mild costvertebral angle tenderness is present. Foley catheter is placed and urine appears red. Lab studies show Na/K 136/3.5 Cl/bicarb 93/6 BUN/Cr 34/2.8 glucose 80 Calcium 6.5 Ketones neg Plasma lactate 2.4 best next step in managment

Pt's presentation is suggestive of ethylene glycol poisoning. Ethylene glycol and methanol poisoning occur when ingested as a substitute for ethanol. The initial symptoms of ingestion of these poisons can mimic ethanol inebriation. However, as alcohol dehydrogenase metabolizes ethylene glycol to oxalic acidand clygolic acid, these metabolites cause profound clinical consequences. Glycolic acid injures the renal tubules, while oxalic acid binds calcium, causing hypocalcemia and calcium oxalate crystal deposition in the kidneys. Once this soccurs, patients develop flank pain, hematuria, oliguria, acute renal failure and anion gap metabolic acidosis. All of these sx are demonstrated in this case. Administration of either fomepizole or ethanol to achieve ADH inhibition is an integral part of tx. This prevents further breakdown of ethylene glycol into its toxic metabolites. Other treatments include sodium bicarbonate to alleviate acidosis and hemodialysis in the case of acidosis and/or end organ damage.

32/M intubated and mechanically ventilated after an opioid drug overdose. he is sedated and passive. ventilator triggers 14 breaths per minute, each delivering 500ml of tidal vol at a peak flow rate of 60L/min. An inspiratory hold is performed for 2 sec following delivery of the tidal volume and airway pressure is measured to be 30cm H2o. The measured pressure most likely reflects which of the following? (looks like a cardiac action potential, plateau is where the inspiratory hold is and is at 30mmH2O

Pulmonary compliance Measurement of airway pressures can be useful in mechanically ventilated patients. The peak airway pressure (the max pressure measured as the tidal volume is being delivered) equals the sum of the resistive pressure (flow x resistance) and the plateau pressure. Peak airway pressure = resistive pressure + plateau pressure The plateau pressure is the pressure measured during an inspiratory hold maneuver, when pulmonary airflow and thus resistive pressure are both 0. It represents te sum of the elastic pressure and positive end-expiratory pressure (PEEP) Plateau pressure = elastic pressure + PEEP Elastic pressure is teh product of the lung's elastance and teh volume of gas delivered. Because elastic recoil is inversely related to lung compliance, the elastic pressure can be calculated as tidal volume/compliance. Decreased compliance (eg pulmonary fibrosis) causes stiffer lungs and higher elastic pressure. Increased peak pressure associated with an unchanged plateau pressure suggests a pathological process causing increased airway resistance such as bronchospasm, mucus plug, or endotracheal tube obstruction. Elevation of both peak and plateau pressures indicates a process causing decreased pulmonary compliance, such as pulmonary edema, atelectasis, pneumonia or right mainstem intubation.

62/M brought to ED after losing consciousness at work. Reports difficulty walking over the past couple of days due to an infected wound on his right foot. PMH diabetes mellitus and hyperlipidemia. BP 80/40, pulse 120/min regular. Skin cold and clammy. Right heart cath RAP, mean 18mm (n 0-8) pulm art pressure 43/21 (n 15-28/5-16) Pulm cap wedge pressure 9 (n 6-12) most likely diagnosis?

Pulmonary embolism- hemodynamic parameters indicate Pulm HTN likely secondary to causes such as left heart disease, copd, and PE. the sudden symptom onset adn recent immobility due to the foot infection make PE a more likely possibility. Depending on teh size of the embolus, PE can occlude part of the pulmonary artery to increase right atrial, right ventricular, and pulmonary artery pressures. This results in hyperdynamic left vent fxn with an increased cardiac index. HOwever pulm cap wedge pressure and systemic vasc resistance are not generally affected. Massive PE usually causes right atrial pressure > 10 mm Hg and pulmonary artery pressure >40mm Hg.

56/F brought to ED with SOB, begans suddenly 2 hrs ago while she was enjoying her favorite tv show. REports sharp left-sided chest pain that worsens with cough. PMH includes DM for the past 10 yrs and HTN for the past 6 yrs. Fam hx is significant for heart disease in her father who died at age 40. Her meds include enteric coated asa, lisinopril, and glipizide. SShe has a 30 pack year hx, but doesn't currently somke. PE: acute distress, sweating profusely. Temp 100.5, pulse 140/min, irregular, resp rate 30/min, bp 110/60, O2 sat 84% on room air, JVP wnl and lungs clear. Serum: hematocrit 40%, WBC 11,600, Plt 190. CXR unremarkable, ECG irregular RR intervals, with no definite P waves and narrow QRS complexes. Which is the most likely cause of her sx?

Pulmonary embolism- nonspecific and highly variable sx, but patient's acute onset SOB and pleuritic chest pain are the 2 most common sx of PE, occurring in 75-66% of patients. Hemoptysis occurs in <20% of cases, and leg sx (which support the dx by suggesting concomitant DVT) are present in <30%. She also has multiple PE findings- tachypnea, tachycardia and low grade fever, which are present in 70, 30 adn 15% of cases respectively. She doesn't have the classic findings of PE on ECG (S1, Q3, T3) or CXR (hampton's hump, westermark's sign), but again such findings are present in only the minority of cases. The ECG adn CXR findings described here are inconsistent with the other answer choices provided. Low o2 sat and afib are associated with poor prognosis.

34/F hemoptysis, severe right sided pleuritic type chest pain x 2d. low grade fever, diarrhea and lethargy x 1 week. on methodone for IVDH, 20pack years, HIV, Hep C. Last CD4+ count was 350, 2mos ago, PPD showed 2mm of induration. PE temp 100.6, tachycardia, rest ok. Breath sounds are diminished at right lung base. dx?

Pulmonary embolism- patient had a GI illness that caused dehydration- a risk factor for venous thrombosis due to hemoconcentration. Acute onset pleuritic chest pain, hemoptysis, tachycardia are suggestive of PE. Hemoptysis is due to pulmonary infarction. Low grade fever and mild leukocytosis are also common in pulmonary embolism. Chest CT shows characteristic wedge-shaped pleural based opacification that is likely to occur distal to a completely occluded pulmonary artery. Pulmonary infarct areas may also occasionally be seen on CXR as hampton's hump. Pulmonary artery filling defects are usually visible on contrast-enhanced CT scans. In addition, PE are common cause of both transudative and exudative pleural effusions. This pts ct scan shows an accompanying unilateral, right sided pleural effusion. `

45/F 3 month history of fatigue, exertional dyspnea, and non-productive cough. She has also been having difficulty swallowing. Her only other medical problems are Raynaud's phenomenon, heartburn and high blood pressure. On examination, diffuse thicekning of the skin with telangiectasia is noted. Her current medications include amlodipine, enalapril, and ranitidine. What is the most probable pathologic mechanism of her pulmonary complaints?

Pulmonary fibrosis. Patient most likely has systemic sclerosis- a wide range of pulmonary complications can occur in patients with systemic sclerosis. They affect up to 2/3 of patients with this condition. The most common underlying mechanism of pulmonary complications is interstitial fibrosis. It develop sin abou t40% of patients with diffuse disease. Pulmonary vascular lesions can develop con comitantly with interstitial fibrosis but isolated pulmonary htn without interstitial fibrosis occurs in less than 10% of patients. Aspiration of gastric content with resultant pna due to esophageal dysmotility is less common than interstitial fibrosis. The risk of bronchogenic carcinoma is increased in pts with systemic sclerosis, but it is not the most common cause of pulmonary complications. Restriction of chest movements due to extensive thoracic skin fibrosis is rare.

Manifestations of sarcoidosis

Pulmonary: bilateral hilar adenopathy, interstitial infiltrates Ophthalmologic: anterior uveitis (iridocyclitis or iritis), posterior uveitis Reticuloendothelial: peripheral lymphadenopathy, hepatomegaly, splenomegaly Musculoskeletal: acute polyarthritis (esp the ankle joints), chronic arthritis with periosteal bone resorption Central nervous system/endocrine: central diabetes insipidus, hypercalcemia Lofgren's syndrome: Erythema nodosum, hilar adenopathy, migratory polyarthralgias, fever

Oral Leukoplakia

Reactive precancerous lesion that represents hyperplasia of the squamous epithelium. Granular texture, non-indurated, not-removed by scraping. Risk factors: smokeless tobacco and alcohol, 1-20% of lesions progress to squamous carcinoma within 10 years. Reversible after cessation of tobacco use.

Idiopathic pulmonary fibrosis

Restrictive lung disease of unknown etiology. Chronic inflammation of the alveolar walls causes progressive widespread fibrosis and destruction of the normal lung architecture. Patients present with chronic progressive dyspnea, nonproductive cough and digital clubbing. Fever and chest pain are typically absent. Examination demonstrates dry, end-inspiratory crackles. PFTs in patients with this condition show a restrictive pattern (decreased TLC, FEV1 and FVC; normal FEV1/FVC). The diffusing capacity is progressively reduced, largely due to ventilation/perfusion mismatch, resulting in an increased A-a gradient. Chest x rays in IPF typically demonstrate decreased lung volumes, airway fibrosis giving a 'honeycomb' pattern and pulmonary vascular congestion most evident in the hilum.

44/asian immigrant- persistent cough and dyspnea on exertion x 3 mos. No fever, chills, runny nose, sputum production. Over the past year he has had progressively worsening shortness of breath and is unable to sleep lying flat. He has no chest pain or diaphoresis but he has had palpitations in the past. He does not smoke or drink alcohol. The patient moved to the US 10 years ago. He is alert but in mild distress. His temp is 98, bp is 110/70, pulse 100/min. BMI 34. Heart sounds are distant due to body habitus. Lungs show crackles. CXR reveals an enlarged cardiac silhouette with vascular congestion. Left main stem bronchus appears to be elevated. There is no other visible lung pathology. ECG shows irregularly irregular rhythm. Pathophysiology is related to?

Rheumatic heart disease Patient's presentation suggests Mitral stenosis. MS is most commonly due to rheumatic fever, which typically occurs during childhood but can happen at any age. There can be a latent period of several years before symptom onset (usually in the 4th or 5th decade of life). Typical sx include gradual and progressively worsening dyspnea on exertion, orthopnea, and hemoptysis (due to pulmonary edema). Sx are usually precipitated by exercise or conditions causing tachycardia (eg fever, anemia, pregnancy) Auscultation shows a loud first heart sound, opening snap after S2 (best heard at the apex), and a low-pitched diastolic rumble best heard at the cardiac apex (patient lying on the left side in held expiration). MS causes eventual backflow of blood into the left atrium, leading to elevated left atrial and pulmonary vascular pressures. This typically progresses over years to cause left atrial enlargement, which can compress the recurrent laryngeal nerve to cause persistent cough or hoarse voice. The enlargmeent can also displace the left main stem bronchus, as seen in this patient's x-ray. About 70% of these patients develop atrial fibrillation which would explain the palpitations and irregularly irregular rhythm noted on this patient's ecg.

AIDS most common middle ear pathology

Serous otitis media- due to the auditory tube dysfunction arising from HIV lymphadenopathy or obstructing lymphomas. Serous otitis media is characterized by the presence of a middle ear effusion without evidence of an acute infection. Conductive hearing loss is the most common symptom experienced by patients with serous otitis media, and examination typically reveals a dull tympanic membrane that is hypomobile on pneumatic otoscopy.

35/M SOB, fever, malaise. PMH 2 yrs of recurrent sinusitis. Former smoker and has an occasional glass of wine. Temp 101.1, bp 110/65, pulse 110, rr 22. Ill appearing male in mild respiratory distress. Patchy rales are appreciated on lung auscultation. CXR reveals multpile nodular densities bilaterally. Serum cr is 2.7 mg/dL, UA shows RBC casts. What would be most helpful in diagnosing this condition?

Serum antineutrophilic cytoplasmic antibody The pt's combo of kidney disease and upper and lower resp tract disease suggests granulomatosis with polyangiitis (Wegener's) GPA. is a systemic vasculitis of small-and medium sized arteries with highest incidence among caucasians ages 30-50. Upper airway involvement may cause bloody/purulent nasal discharge, oral ulcers, and sinusitis. Lower airway sx include dyspnea, cough and hemoptysis. The renal disease in GPA genearlly manifests as renal insufficiency, microscopic hematuria and RBC casts (rapidly progressive glomerulonephritis). Systemic sx like fever, weight loss, and fatigues are also common. CXR may demonstrate nodular densities and alveolar/pleural opacities. In all pts with suspected GPA, the serum should be tested for antineutrophilic cytoplasmic antibody as it is positive in >90% of affected individuals. Biopsy from a site of active disease (preferably nasopharyngeal) makes the definitive diagnosis. Diagnosis is made by c-ANCA positivity and tissue biopsy. Treatment involves high dose corticosteroids and cytotoxic agents.

45/f brought to the ED, empty bottle of med, en route to ER suffered a tonic clonic seizure, pmh significant for major depression and chronic back pain. Temp 100.9, bp 90/70, pulse 120/min, resp 16. pupils 8mm in size bilaterally. Skin warm and flushed. Lungs clear to ausc, abdomen soft and nontender, bowel sounds decreased, no neck stiffness. EKG shows QRS duration of 130msec, change form her previous ekg a month ago. What is the most appropriate next step in mgmt?

Sodium bicarbonate. Pt's hx of depression with presenting sx indicates she most likely OD'd on TCAs. TCAs can cause hyperthermia as well as other anticholinergic effects. INcluding dilated pupils, and intestinal ileus. IT can also caand decreases the incidence of ventricular arrhythmia. use seizures. TCA overdose decreases myocardia conduction velocity, leading to QRS prolongation and risk of ventricular arrhythmia. However, the major cause of mortality in TCA overdose is believed to be secondary to TCA-induced hypotension. The first priority when encountering a pt with TCA overdose is to secure their airway, breathing and circulation. In cases of hypotension, QRS prolongation, and ventricular arrhythmia, sodium bicarb is administered. Sodium bicarb improves systolic bp, narrows the QRS complex

MOA of sodium bicarb in treating TCA overdose

Sodium load of sodium bicarbonate will alleviate depressant action on sodium channels. Among the many significant cellular effects of tricyclic antidepressants, the inhibition of cardiac fast sodium channels is responsible for QRS prolongation. QRS prolongation can lead to ventricular arrhythmias and thus narrowing of the QRS interval is a critical aspect of treatment in TCA intoxication. IN patients with a QRS interval of greater than 0.10 seconds, the physician should administer sodium bicarbonate. Sodium bicarbonate reverses the prolongation of the QRS interval by increasing the extracellular sodium concentration. Besides, alkalinization of the serum decreases drug avidity for the sodium channels.

apical lung tumor causing horner syndrome, pancoast syndrome, hoarse voice, svc syndrome. Pain, paresthesias and/or weakness of the arm

Superior sulcus tumor apical tumor that can cause compression of the sympathetic trunk (horner), brachial plexus (pancoast) right recurrent laryngeal nerve (hoarse voice), svc syndrome. Pain, paresthesias and/or weakness of the arm. Specifically, Pancoast syndrome is characterized by shoulder pain radiating into the arm in an ulnar distribution and is caused by tumor invasion of the 8th cervical and first thoracic nerves.

48/F lifetime nonsmoker is found to have a lung nodule on cxr for evaluation of a dry cough. The cough has since resolved. She currently has no complaints and says that she is full of energy. The pt was dx with breast cancer 3 years ago and underwent a right sided mastectomy and combination chemotherapy. CT of the chest reveals a 2cm peripheral, round lesion in the right lower lung lobe completely surrounded by lung parenchyma. The borders are irregular and there is no calcification. There are no other lung lesions or lymph node enlargement. Which of the following is the best next step in management of this patient?

Surgical resection. Solitary pulmonary nodule is defined as a lesion (usually <3 cm) that is within and completely surrounded by pulmonary prenchyma. The first step in evaluating is to determine the probability of malignancy. This patient has a PMH of node-positive breast cancer and now presents with an irregular and poorly defined nodule. These features indicate a high probability that the nodule is a malignant lesion. She should have a complete surgical excision of the nodule as a potentially curative procedure. Surgical excision is also recommended in pts with lesion growth on serial imaging, positive 18-fluorodeoxyglucose positron emission tomography (FDG-PET) scans, and biopsy-proven malignant nodules.

34/farmer brought to hosp after attempting suicide. His body and clothes are soiled with vomitus. He is short of breath and appears agitated. His family reports no previous medical history or regular use of prescription meds. His temp is 98, bp is 110/60 pulse is 50/min and resp are 22/min. His o2 sat is 86% on room air. Exam shows watering of the eyes and 1mm pupils, bilaterally. Lung examination shows widespread ronchi with prolonged expiration. Abdominal examination shows increased bowel sounds. Neurologic examination shows muscle fasciculations. What would be the most appropriate next step in management of this patient.

This farmer has organophosphate poisoning. In organophosphate poisoning, acetylcholinesterase is rendered non-functional leading to symptoms of cholinergic excess. The common presentation includes bradycardia, miosis, bronchorrhea, muscle fasciculations, salivation, lacrimation, diarrhea and urination. To counteract the effects of organophosphate poisoning, atropine should be administered immediately. It acts by competing with acetylcholine at the M receptors, and would therefore reverse the patient's sx. Of equal importance is the immediate removal of the pt's clothing (since it is soaked with vomitus to prevent continued absorption of organophosphates through the skin.

Common complication of chronic beclomethasone use

Thursh- local delivery of corticosteroids to airways by inhalation is a cornerstone of chronic therapy for asthma due to the low incidence of adverse effects. Most common adverse effect asso with the use of any inhaled corticosteroid is oropharyngeal candidiasis (oral thrush). High doses can lead to increased systemic absorption adn can produce adrenal suppression, cataract formation, decreased growth in children, interference with bone metabolism and purpura. However these systemic effects are dose-dependent and occur in pateints who are on high-dose inhaled steroids for prolonged periods of time.

Common causes of pleural effusions- transudate vs. exudate

Transudate: -CHF -Cirrhosis -Nephrotic syndrome - Peritoneal dialysis Exudate -infections -malignancy -connective tissue diseases -inflammatory disorders -mvt of fluid from abdomen to pleural space -coronary artery bypass sx -pulmonary embolism

56/Obese man to ED complaining of acute onset sob. Twisted his ankle 6 d ago and has had limited mobility since. Other med problems include type 2 dm, htn, chronic kidney disease, right knee osteoarthritis. His meds include insulin, amlodipine, and low dose asa. BP is 110/60 and pulse 110. His hb level is 11.2 and platelet count is 230K. The estimated glomerular filtration rate is 20ml/min/1.73. Ventilation perfusion scan shows a right upper-lobe perfusion defect with good ventilation. Best initial treatment for this patient?

Unfractionated heparin. Patient has confirmed pulmonary thromboembolism. Untreated PE has a mortality risk of up to 30% due to recurrent embolism. As a result, immediate anticoagulation is required unless contraindicated. There are many anticoagulant options available. Low molecular weight heparin (enoxaparin), fondaparinus (inj factor Xa inhibitor) and rivaroxaban (oral factor Xa inhibitor) cannot be used in patients with severe renal insufficiency (estimated glomerular filtration rate <30mL/min/1.73m2) as reduced renal clearance increases anti-Xa activity levels and bleeding risk. Unfractionated heparin is recommended in pts with decreased estimated gfr as it is more convenient to monitor its therapeutic level via activated partial thromboplastin time (aPTT). once the heparin produces therapeutic anticoagulation (goal PTT > 1.5-2 times normal), warfarin is initiated. Warfarin can take up to 5-7 days to reach therapeutic levels. It also inhibits proteins C and S (anti-thrombogenic proteins) and can be thrombogenic without a second anticoagulant (eg heparin) as a 'bridge' after reaching a therapeutic INR< hep can be stopped, and warfarin can be continued long term. Rivaroxaban is an oral anticoagulant with immediate onset of action (unlike warfarin. Therefore no bridging with heparin is indicated. Unfortunately, this is not an option for patients with severe renal insufficiency.

40/M brought to ED for retrosternal and epigastric pain s/p ingesting unknown amt of lye (drain cleaner) 45 mins ago. PMH sig for major depression and suicide attempt. Unable to swallow his saliva and is drooling. Temp 98.2, bp 120/70, pulse 110, resp 20. Exam shows oropharyngeal erythema and edema. Lungs are clear to auscultation. A bd examination reveals tenderness at the epigastrium without rebound or guarding. CXR shows no abnormalities. IV hydration is started. What is the most appropriate next step in treatment?

Upper GI endoscopy. The patient has ingested lye (sodium hydroxide), a strongly alkaline solution, in an apparent suicide attempt. Esophageal damage induced by lye ingestion begins almost instantaneously. Alkaline solutions cause liquefactive necrosis of the esophageal wall, which can lead to perforation and mediastinitis. Patients often present with retrosternal/epigastric pain, hypersalivation and odynophagia/dysphagia. Patients should be hospitalized, given IV hydration, and receive serial abdominal and CXRs. Endoscopy should be performed expeditiously to assess the extent of esophageal injury and to determine if any further management is needed. If perforation is suspected, a Gastrografin study should be performed.

confusion, nystagmus, ataxia, ophthalmoplegia

with thiamine deficiency = wernicke encephalopathy. Korsakoff syndrome is the chronic complication with short term memory loss and confabulations.

Treatment of mild to moderate asthma exacerbation

usually responds to oxygen and inhaled short-acting beta agonists (SABAs) to effectively reverse airflow obstruction. Patients who do not respond require systemic corticosteroids (usually oral)

AE: Hyperkalemia, angioedema, cough

ACE inhibitor like lisinopril

Rhinitis, post nasal drainage, wheezing following naproxen

Aspirin exacerbated respiratory disease- commonly associated with the dev'p of nasal polyps. AERD consists of the features: asthma, chronic rhinosinusitis with nasal polyposis, and bronchospasm or nasal congestion following the ingestion of ASA or NSAIDS. Dx can be made clinically when all 3 sx are present. Bland tasting food = secondary to anosmia.

Common drug that cuases tinnitus

Aspirin usually causes tinnitus. At very high doses- 6-8g/day, hearing loss.

increased heart rate, increased blood pressure, dilated pupils, euphoria, sense of self confidence, increased arousal, impvoed performance on tasks and alertness and vigilence.

Cocaine intoxication

Good antibiotic for outpatient community acquired pna where the macrolide resistance is suspected

Doxycycline

Consolidation of the lung sounds like

Dullness to percussion. prominent expiratory component. bronchial breath sounds (assuming patent airways). Egophony would be positive, crackles are usually heard.

Pulmonary thromboembolism and has a hx of recurrent 'unexplained' DVT of lower extremities.

Factor V leiden is recognized as a relatively common cause of such a condition. Factor V Leiden is a result of a point mutation in a gene coding for the coagulation factor V. As a result of this mutation factor V becomes resistant to inactivation by protein C, an important counterbalance factor in hemostatic cascade. The prevalence of factor V leiden may be as high as 5-6% of the population.

Fixed upper airway obstruction effect on flow-volume loop

Flow limitation with both inspiration (below the horizontal line) and expiration (above the horizontal line). Since her sx started in a restaurant, this patient's laryngeal edema is most likely asso with an allergic reaction to food. She thus requires epinephrine, systemic corticosteroids, and antihistamines.

Drugs that cause ototoxicity

Furosemide/loops- associated with reversible or permanent hearing impairment, reversible deafness, and/or tinnitus. Dose dependent. Patients with renal failure experience hearing loss/deafness at lower doses. Other drugs: aminoglycosides: Genitmycin, tobramycin, streptomycin, neomycin

Vasculitis, upper and lower airway granulomatous inflammation and glomerulonephritis

Granulomatosis with polyangiitis (wegener's)

Intense vertigo with gaze abnormalities, limb ataxia, sensory loss, and Horner's syndrome

Lateral medullary infarction aka Wallenberg syndrome

common cause of CAP in patients with COPD

Hemophilus influenzae. Moraxella catarrhalis is also associated with COPD but less common.

Calcified nodes in lung, mediastinum, spleen, liver, cxr central or target calcification, solitary nodule sometimes. Mediastinal lymph node enlargmeent

Histoplasmosis- most common fungal infection in the USA. Yeast infection acquired by inhalation, usually self limited.

Teenage male with nasal drainage, epistaxis, nasal obstruction

Juvenile nasal angiofibroma- rare, benign tumor of the nasopharynx that can cause nasal obstruction and nasal drainage, and usually results in epistaxis.

Predominant nasal congestion or stuffiness, postnasal drip (dry cough) and no specific identifiable triggers

Nonallergic rhinitis aka vasomotor rhinitis Dx is typically clinical. NAR pts usually have negative testing for allergens. Those with prominent rhinorrhea and/or postnasal drip sometimes respond to first-generation oral H1 antihistamines (eg chlorpheniramine) but rarely ever to antihistamines without anticholinergic properties (eg loratadine). These patients are best managed with either a topical intranasal antihistamine spray (eg azelastine, olopatadine) or intranasal glucocorticoids. Moderate to severe sx usually require BOTH intranasal antihistamines and intranasal glucocorticoids. Nasal cytology usually shows predominant eosinophils and increased numbers of mast cells. Not essential for diagnosing NAR.

Primary risk factor for bronchogenic carcinoma

Smoking

DOC for uncomplicated cystitis adn sinusitis

Trimethroprim/sulfamethoxazole

DLco lowered

interstitial lung disease

AE: Hypotension, photosensitivity, hypercalceimia, sulfa allergy

HCTZ

Therapeutic INR for patients with idiopathic VTE or afib

2-3

PCP in HIV patients at CD4 counts of

<200

Therapeutic INR for prosthetic heart valves

2.5-3.5

Herpes simplex 1 in the oral cavity

gingivostomatitis- multiple vesicular lesions with an erythematous and inflammatory base and erythematous border within the oral cavity and perioral area. HS1 doesn't cause whit plauque.

Initial therapy for PAD

Aggressive risk factor modification with counseling for smoking cessation, lipid lowering therapy, and evaluation/tx of HTN and DM. Enroll the patient in a supervised exercise program- minimum of 12 weeks with 30-45 minutes of exercise at least 3x/week for all patients with claudication. Goal is to reproduce claudication sx during each session. Supervised exercise programs have been shown to reduce sx and improve max walking distances. Percutaneous or sx revascularization is generally reserved for pts who have persistent sx despite exercise and/or pharm therapy. Warfarin doesn't improve claudication sx.

Reflex hyperactivity in certain parts of the brain that manifests as anxiety, insomnia, tremors, diaphoresis in teh first 6-24 hours

Alcohol withdrawal. hallucinations and withdrawal seizures can also occur in the first 48 hours in these patients. TH emost serious affect of alcohol withdrawal is delirium tremens, which occurs in 5% of untreated patients. DT occurs after 48-96 hours, adn consists of hypertension, agitation, tachycardia, hallucinations and fever, with a mortality rate of up to 5%. Treat with benzos, chlordiazepoxide = librium.

Good synergism against gram negative aerobes

Ampicillin and gentamicin combo has good synergism against gram neg aerobes. It can be used for abdominal infections in combination with metronidazole.

Rinne normal bilat, weber to right

left sensorineural

CHF and pleural effusions

CHF commonly causes transudative effusions, however 25% of effusions can meet exudative criteria if the patient has received aggressive diuretics prior to thoracentesis. These effusions are usually bilateral (61%) but can be unilateral on either the right (27%) or left (12%) side.

PE of COPD exacerbation

COPD exacerbation typically shows widespread bilateral wheezes, and ABG findings include respiratory acidosis and hypoxia.

Steps for evaluating possibly lung malignancy

CXR, CT, Bronchoscopic or CT guided biopsy

34/M brought to ED by neighbor, lying on floor beside an empty bottle of unknown subastnace. Patient is conscious nad alert but in severe pain. Temp, bp and pulse wnl, resp 20. Abdomen is benign, normal bowel sounds. Pupils 5mm bilaterally. Tongue is white, heavy drooling of saliva is noted and unable to swallow. Which is the most likely explanation of patient's symptoms

Caustic poisoning. Caustic ingestion is least likely to affect patient's cognition- leads to damage of the tissue lining the GIT, manifested by necrosis, edema, scarring and severe pain. White tongue, heavy salivation and dysphagia are all results of this process. Several esophageal and stomach ulceration may also occur and physicians should monitor for indications of peritonitis and mediastinitis

dry cough and systemic symptoms that last for months. CXR shows bilateral ground glass infiltrates

Cryptogenic organizing pneumonia

GERD and asthma

GERD occurs in 30-90% of people with asthma. Change in voice quality, laryngitis, heartburn, regurg, dysphagia, chest pain. Gerd can exacerbate airflow obstruction in asthmatics through increased vagal tone, heightened bronchial reactivity, and microaspiration of gastric contents into the upper airway.

Most common causes for severe sore throat, drooling, progressive airway obstruction

Haemophilus influenzae and strep pyogenes. Harsh shrill = stridor, which can occur in some pts with epiglottitis. Epiglottitis is a medical emergency and rapid treatment must be initiated to prevent obstruction of the airway. Emergency laryngoscopy is typically required in patients with epiglottitis to ensure adequate protection of the airway.

Gram negative bacilli causing pneumonia in infants, elderly, alcoholics, immunocompromised.

Klebsiella pneumonia, aka friedlander's pna. Gram neg bacilli accounts for <2% of CAP but account for MOST of the nosocomial infections and have high mortality rates. Some of the common GNB causing pna are e coli, klebsiella, pseudomonas, enterobacter, proteus, serratia and acinetobacter. They esp have neutropenia. Usual pathophysiology is colonization of the oropharynx, followed by micro aspiration of upper airway secretions. Friedlander's pna most frequently affect the UPPER lobe and produce currant jelly-like sputum with tissue necrosis and early abscess formation and a fulminant course. Kleb is the most common organism responsible for PNA in alcoholics. It is an encapsulated GNB and grows as mucoid colonies.

43/F with CHF, RA, Hep C with early liver cirrhosis complains of difficulty breathing. Temp 100F, BP 126/72mm, pulse 97, resp 28. Pulse ox is 94% on room air. PE shows dullness to percussion at the right lung base. CXR shows moderate-size right pleural effusion and can't rule out underlying infiltrates. Thoracentesis shows pleural fluid with gluco f 28 and lactate dehydrogenase of 252 (nml 100-250). What explains a pleural fluid glucose of <30?

Likely PNA with parapneumonic effusion. Pleural effusionsa re divided into transudates and exudates. Transudates are due to an imbalance between hydrostatic and oncotic pressures that increases fluid mvt across the caps into the visceral pleural and pleural space. Transudative fluid requires no further intervention except for tx directed at teh underlying disease. Exudative effusions are due to pleural and lung inflammation resulting in increased capillary and pleural membrane permeability. Exudative effusions require more extensive diagnostic investigation. The low pleural glucose also indicates an exudative pleural effusion. Pleural fluid glucose <60 mg/dL is usually due to rheumatoid pleurisy, complicated parapneumonic effusion or empyema, malignant effusion, tuberculosis, pleurisy, lupus pleuritis, or esophageal rupture. Pleural glucose <30mg/dL suggests an empyema or rheumatic effusion. Glucose concentration in empyema is decreased due to the high metabolic activity of leukocytes (and/or bacteria in the fluid)

increased appetite, tachycardia, tachypnea, hypertension, dry mouth and conjunctival injection. Also decreased reaction time, impairs attention, concentration and short term memory. Impairment of cognition, judgement and coordination lasting longer

Marijuana intoxication. Can increase the risk of motor vehicle accidents

Fever, muscle rigidity, autonomic instability and mental status chang.e Elevated creatine kinase, leukocytosis and electrolyte abnormalities are also common

Neuroleptic malignant syndrome

Nosocomial pneumonia patients

Often- MRSA- use vancomycin

aggressive behavior, ataxia, mild hypertension, multidirectional nystagmus, impaired judgement, tachycardia

PCP intoxication

indications for oxygen therapy in COPD

PaO2 < 55, SaO2 < 88, hematocrit > 55%, or evidence of cor pulmonale

33/M involved in MVA with numerous rib fractures. Hospital course complicated by difficulty with deep breathing and later dev'p PNA. CXR later confirmed that patient had developed a paraPNA effusion. Which one of the following lab tests on the pleural fluid is currently thought to be the most helpful in determining the need for chest tube placement in parapneumonic effusion?

Parapneumonic effusions usually occur from pneumonia. The fluid may be sterile in the initial stages and resolve with antibiotic therpy; however, in a few cases, the patient will continue to have elevated temperatures, pleuritic chest pain, and dyspnea. CT scan will identify the fluid collection. The fluid may be aspirated to determine if empyema has set in. The aspirated fluid should always be analyzed for the protein content (exudates have more than transudates) gram stain, celll count, cytology (rule out malignancy), and glucose levels (low in rheumatoid arthritis, tuberculosis, empyema, malignancy and esophageal rupture). The pH of the fluid should always be assessed. Low pH (<7.2) is almost indicative of an empyema and indicates removal of the fluid by thoracostomy. Glucose of less than 60 is also an indication for tube thoracostomy.

Source of PEs

Proximal deep veins (iliac, femoral and popliteal) are the source of >90% of PEs.

Normal or increased FEV1/FVC ratio- with a low VC

Restrictive lung disease

Most common organisms responsible for acute exacerbation of COPD are

S. pneumoniae, H. influenza, and M. catarrhalis.

PE in an ecg

S1 Q3, Tinversion in lead 3.

Drug of choice for pneumocystis pna

TMP-SMX- effective against many gram negative and gram positive agents, but it does not provide significant anaerobic coverage

Tachycardia, diaphoresis, dilated pupils, htn, hyperthermia in od

Serotonin syndrome tends to occur as a result of intentional od, or as a consequence of drug interactions (classically when MAOI's are mixed with other serotonergic agonists). Presentation includes tachypnea, diaphoresis, dilated pupils, htn, and hyperthermia.

Clinical presentation of pancoast tumors

Shoulder pain (most common) Horner's syndrome C8-T12 neurological involvement -weakness and/or atrophy of intrinsic hand muscles -pain and paresthesias of 4th adn 5th digits, medial arm and forearm Supraclavicular lymph node enlargement weight loss Patients can also develop increased sympathetic activity in the contralateral side with flushing and facial sweating during exercise (Harlequin sign). Most pancoast tumors are non-small cell lung cancers. Initial evaluation is CXR. Subsequent CT or MRI can further stage the disease.

Progressive dyspnea, cough, decreased breath sounds and a prolonged expiratory phase

Signs and sx of COPD. Hypoxemia on ABG, pulse ox or hematocrit is common. Smoking is the most important risk factor. Long term supplemental o2 therpy has been proven to prolong survival and improve quality of life in hypoxemic patients with COPD.

bilateral pulmonary hilar adenopathy evident on cxr and numerous other systemic signs and sx

sarcoidosis

CNS depression, cardiac arrhythmias, hypotension, hyperthermia, flushing, diated pupils, decreased bowel sounds, urinary retention on OD

TCA poisoning. Most appropriate indicator of the severity of intoxication is duration of the QRS complex.

Respiratory distress, hypotension, tachycardia

Tension pneumothorax- tracheal and mediastinal displacement to the contralateral side and radiolucence on the affected side. usually shows improvement with chest tubes.

Seizures, hyperthermia, cardiac arrhythmias, hypotension in od

Theophylline intox.

CNS stimulation, GI disturbances, Cardiac toxicity

Theophylline toxicity- accumulation by reduced clearance or decreased metabolism due to saturation of metabolic pathways. Theo is metabolized by the cyt oxidase system in the liver. Inhibition of thsee enzymes by concurrent illness (eg, cirrhosis, cholestasis, respiraotry infections with fever) or drugs (eg cimetidine, cipro, erythromycin, clarithromycin, verapamil) can raise serum concentration and cause toxicity. Symptomso f tox usually manifest as CNS stimulation (eg headache, insomnia, seizures), GI disturbances (eg nausea, vomiting), and cardia ctoxicity (arrhythmia). This patient recently began taking cipro, a drug known to decrease clearance of theophylline. therefore te best next step is to measure serum theo levels to assess for tox.

The first step in determining the etiology of a pleural effusion is to decide if the effusion is a transudate or exudate. Exudate if the fluid protein/serum protein ratio is greater than 0.5, the fluid LDH/serum LDH ratio is greater than 0.6, or the pleural fluid LDH is greater than 2/3 of the upper limit of the normal serum LDH. The patient's pleural fluid protein of 5.2mg/dL is greater than 1/2 of the serum value.

There are a variety of potential causes of an exudative pleural effusion including infection, autoimmn disease and neoplasm. These all cause effusions via *increased capillary permeability, which allows protein and LDH to pass into the pleural fluid. An elevated pleural fluid lymphocyte count, as is seen here, is suggestive of tuberculosis, sarcoidosis, lymphoma, or rheumatoid arthritis. Bacterial infection or lung cancer are less likely in this patient given the negative pleural fluid culture and cytology.

40/M after wife found him alone in a confused state. Admits to suicide attempt, doesn't specify drug. Drowsy and ataxic with blurred vision. PMH sig for asthma, insomnia, depression, substance abuse. Temp 100. BP 130/80, pulse 100, rr 22. Dry mucus membranes and skin, pupils are 8mm bilat. No neck stiffness. Lungs clear to auscultation. Heart sounds WNL. Ab exam shows reduced bowel sounds with no tenderness. Foley placed and 600ml of urine collected over 1 hr. Most likely diagnosis?

This patient's mixture of anti-cholinergic symptoms, drowsiness and confusion are suggestive of diphenhydramine overdose. Diphenhydramine in excess exerts significant anti-histamine and anti-cholinergic effects, including confusion, drowsiness, dry mouth, dilated pupils, blurred vision, reduced bowel sounds and urinary retention. Proper tx for significant od includes administration of physostigmine, a cholinesterase inhibitor which reverses its effects

Ventilation and respiratory alkalosis

Ventilation is defined as the product of the respiratory rate and the tidal volume. Respiratory alkalosis results from hyperventilation. In mechanically ventilated patients with resp alk in the setting of an appropriate tidal volume, the respiratory rate should be lowered. (Reductions in tidal volume can trigger an increased ventilatory rate, potentially exacerbating the situation.)

Coccidiodomycosis is

a fungal infection of the lungs that can cause fever, cough and night sweats. Extrapulmonary manifestations may involve the skin, meninges, and skeleton. Coccidiodomycosis is endemic to the southwestern US, not WI.

Lung abscess on CXR

air fluid level

hyperthermia, mydriasis, delirium, urinary retention, decreased bowel sounds, dry mouth in an od

anticholinergic toxicity

hemoptysis, fever, weight loss, chronic cough, mobile mass, moves with position, apex of lung

aspergilloma- diagnosis is made by finding the hyphae in teh specimen.

outpatient tx of CAP:

azithromycin or doxycycline

Pneumonia severity index

based on med history PE readily available lab and radiographic findings Most common cause of lobar pneumonia in CAP is pneumococcus. Other causes include Hemophilus, moraxella. New generation quinolones (levofloxacin or moxifloxacin) is being extensively used for the inpatient treatment of CAP. Nearly 97% of strep pneumo is sensitive to these drugs. Also these drugs cover the atypical organisms. For the mgmt of outpatient therapy in stable and low-risk patients (no other cardiopulmonary risk factor, not hypoxic), either azithromycin or doxycycline can be used.

OD resulting in Bradycardia, AV block, hypotension and diffuse wheezing

betablocker od. Wheezing is specific to beta blocker toxicity. The most common presentation of beta blocker toxicity is bradycardia and hypotension, which can lead to cardiogenic shock, as indicated by cold and clammy extremities in this patient. Other effects include bronchospasm (beta 2 blockade) as evidenced by diffuse wheezing, neurological effects (delirium and seizures), and hypoglycemia. To reverse the effects of toxicity, atropine and IV fluids are first given. If this fails to improve bp, glucagon is the next agent administered. Glucagon leads to an increase in cAMP and higher levels of intracellular calcium, thereby augmenting cardiac contractility.

lung tumer central located and easily visible with a bronchoscope. Present with cough and recurrent hemoptysis. Slow growing and best prognosis of all lung cancers

carcinoid tumors. Carcinoid syndrome is a rare presentation.

hypertension, agitation, tachycardia, hallucinations, fever with a mortality rate of up to 5%

delirium tremens, occurs after 48-96 hours of alco hol withdrawal. Treat with benzos- chlordiazepoxide (librium)

tremor, rigidity, bradykinesia and gait abnormalities

drug induced parkinsonims

inpatient tx of CAP

levofloxacin or moxifloxacin (newer anti-pneumococcal quinolones)

abx with Excellent streptococcal coverage

new general fluoroquinolones (levofloxacin)

Exercise-induced asthma

obstructive airway disease characterized by dyspnea, cough and wheezing, following exposure to various triggers. Atopic dermatitis and allergic rhinitis are commonly associated conditions. In exercise-induced asthma, the trigger is high minute ventilation of dry, cold air, which stimulates mast cell degranulation and airway constriction. Beta agonists and mast cell stabilizers are both important in the management of exercise-induced asthma. Short-acting-beta-adrenergic agonists used 20 mins prior to exercise are typically sufficient to prevent sx and are considered first line therapy. Long acting beta-adrenergic agonists may be used in children or athletes who engage in athletic activities throughout the day.

agitation, tachycardia, pupillary dilation, often with psychotic and/or dissociative behavior. vertical nystagmus as well in od

phencyclidine poisoning

rinne normal weber left

right senorineural

Causes of recurrent pneumonia involving different region of the lung

sinopulmonary disease (eg cystic fibrosis, immotile cilia) noninfectious (eg vasculitis, bronchiolitis obliterans with organizing pneumonia) immunodeficiency (eg HIV, leukemia, decreased immunoglobulins)

Common side effects of cephalexin

skin rash, vomiting, diarrhea, abdominal pain.

Bronchoalveolar lavage has greatest diagnostic utility in the evaluation of

suspected malignancy and opportunistic infection. It can also be used in the evaluation of a variety of other lung conditions, but with inferior diagnostic yield. The role of BAL in the work-up of suspected PCP is well established. Occurs at CD4 counts <200

Tx of mild persistent asthma

sx >2 days/week, but less than daily, nighttime awakenings 3-4x/month, minor limitation of activities, and normal PFTs should be given a low-dose inhaled corticosteroid as a controller medication, in addition ot the PRN albuterol in haler.

history of alcoholism and recent initiation of fluconazole and moxifloxacin prediposes a patient to

torsades de pointes. Treat with magnesium sulfate. Torsades de pointes is a polymorphic ventricular tachycardia associated with a prolonged QT interval. It commonly occurs in patients with familial long QT syndrome, as well as in malnourished patients predisposed to hypomagnesemia, such as alcoholics. For patients with this rhythm, it is important to discontinue any offending agents, and administer magnesium sulfate Certain drugs (TCAs), certain antiarrhythmics (amiodarone, sotalol) and anti-infective agents (moxifloxacin, fluconazole) predispose people. Also malnourished patients who are hypomagnesemic.

35 y/o from WI w/fever, night sweats, productive cough and an unintentional 17-lb weight loss over past 3 mos. Several days ago, multiple skin lesions. No PMH/meds/tobacco/etoh/drugs. Works outdoors wood cutting and in construction. PE reveals a man of med build in no apparent distress. His temp 101.1, bp 120/68, pulse 86, resp 14. Skin multiple, well-circumscribed, verrucous, crusted lesions. CXR shows left upper lobe consolidation and 2 lytic lesions in the anterior ribs. Most likely cause?

Blastomycosis. 3 mo history of low grade fever, night sweats, productive cough and weight loss could be explained by chronic infection, malignancy or rheumatologic disease. Skin involvement, lytic bone lesions and geographic location make blasto the most likely cause. Blasto is a fungal infection that occurs most often in the vicinity of the great lakes, mississippi river and ohio river basins (WI has the highest infection rate). The pulm symptoms and chest x-ray findings of Blasto may resemble tuberculosis and histo. However systemic blasto may cause characteristic ulcerated skin lesions and lytic bone lesions. Broad based budding yeast grown from the sputum confirm the dx. Itraconazole or amphotericin B may be used to treat symptomatic disease.

65/M with oxygen dependent COPD, chronic afib, depression has sx of increased dyspnea and worsening cough pattern. Recent hx significant for a gradual worsening of his baseline lung disease over the past month, which had been treated by his outpt doctor with increased frequency of inhaled beta-agonist and azithromycin. This am had severe SOB that was unresponsive to 'stacked' home nebulizer tx. ER physician notes pt is in moderate severe resp distress. His temp 99, bp 150/90, pulse 110/min, resp 28/min. accessory m use was noted. Lung exam shows diffuse ronchi and wheezing. Pulse ox showed 80% sat on room air. ED doc gave neb, and on 5 L o2. What else should be considered in this patient?

COPD- acute exacerbation. Acute episodes are typically managed with ipratropium and albuterol nebulization and systemic steroids. Most commonly used parenteral steroid is methylprenisolone.

55/F 2 years of episodic cough productive of yellow sputum. First episode ~3 weeks with chest congestion, cough productive of purulent sputum, sob. dx with bronchitis, given abx. patient has since had 6 more episodes, sometimes blood tinged, large amts of yellow sputum. SOB and sinus congestion. improved with abx, daily cough worse past 2 weeks. PE shows diffuse ronchi and wheezes and coarse crackles in bilat lung bases. CXR shows linear atelectasis in mid and lower lung fields bilaterally.

Clinical features of bronchiectasis - cough with sputum production most days of the week - rhinosinusitis - dyspnea, hemoptysis, pleurisy - wheezing, cracklers, digital clubbing Etiologies: -airway obstruction -congenital (eg cf/alpha1antitrypsin) -immunodeficiencies (eg hypogammaglobulinemia) -post-infectious (Eg aspergillus, viral, tb) -rheumatic and systemic diseases eg RA, sjogren's) Toxic inhalation/aspiration Evaluation CBC with diff immunoglobulin quantification sputum culture/smear for bacteria, fungi, tb high resolution ct pulmonary function tests Bronchiectasis results when damage occurs to the bronchial walls form inflammation or infection. Airway damage leads to further infection. chronic productive cough with mucopurulent sputum, dyspnea, hemoptysis, fatigue, weight loss. associated with a larger volume of sputum (>100ml/day), recurrent fever, hemoptysis, and pseudomonas aeruginosa infections. Pts with chronic bronchitis usually complain of nonpurulent expectoration. PE findings include crackles, ronchi, and wheezes on lung exam. CXR is not sensitive or specific for bronchiectasis but can reveal nonspecific findings like linera atelectasis, dilated and thickened airways and irregular peripheral opacities. High resolution CT is preferred for dx and can show bronchial dilation, lack of airway tapering, and bronchial wall thickening on CT scan. After bronchiectasis is confirmed, all pts require sputum analysis. Bronchoscopy is recommended in pts with focal disease to evaluate for localized airway obstruction. Pts with diffuse disease should be assessed for underlying systemic abn, including congenital disorders and immue-mediated dysfunction. Tx involves addressing underlying etiology, corticosteroids, and macrolides to reduce airway inflammation and pharmacologic agents and chest physiotherapy to mobilize secretions. Exacerbations should be treated with abx tailored to sputum microbiology results. Surgical resection and transplantation may be necessary in severe disease.

Clinical features of asbestosis

Clinical presentation: prolonged exposure, sx develop > 20 yrs after initial exposure, progressive dyspnea over mos, bibasilar end-inspiratory fine crackles and clubbing, increased risk for malignancies. Dx: Hx and clinical findings of exposure (eg pleural plaques on cxr virtually pathognomonic) Interstitial fibrosis on imaging or histology and /or pulmonary fxn tests with restrictive pattern. Exclusion of other diseases. Cor pulmonale can eventually develop with peripheral edema, hepatojugular reflux, jugular venous distension, and/or a right ventricular heave. Typical chest x ray findings include interstitial abnormalities of the lower lung fields and pleural plaques (the hallmark of the disease). As in other forms of interstitial lung disease, pulmonary function tests show a restrictive pattern (decreased lung volumes with normal or elevated forced expiratory volume in 1 second/forced vital capacity fev1/fvc ratio) accompanied by reductions in diffusion lung capacity and pulmonary compliance.

Pulmonary HTN

Defined as a MAP of greater than 25 at rest or 30 with exercise. Seen following the narrowing of precapillary vessels, the loss of the pulm capillary bed, or passive backpressure form the post capillary vessels form any cause. Classified as: 1. PH asso with disorders of resp system, Hypoxemia or both 2. PH due to pulmonary venous HTN (LVH disease, mv disease, pulmonary veno-occlusive disease) 3. PH following chronic thromboembolic disease 4. Pulmonary atertial htn (primary pulmonary hypertension, pulmonary htn associated with vasculopathy) 5. pulmonary hypertension due to disorders directly affecting the pulmonary vasculature. Dyspnea, weakness and fatigue are early complaints. Followed by chest pain, hemoptysis, syncope, or hoarseness (due to compression of the recurrent laryngela nerve). RV failure develops late in the disease and manifests as right ventricular heave, jvd, tender hepatomegaly, ascites, edema, etc. CXR shows enlargement of pulmonary arteries with rapid tapering of the distal vessels and enlargements of the RV. EKG may show right axis deviation, 2/2 to right ventricular strain and hypertrophy due to pulmonary htn. Untreated ph should eventually lead to cor pulmonale.

45/M with 2 days of bilateral hand pain that is most severe in his wrists. PE reveals bilat wrist tenderness, hickening of the distal fingers and v convex nail beds. Nicotine staining - 2 packs/day x 25 years. Chest exam reveals decreased breath sounds and prolonged expiratory phase. Data entry job he just started. Most appropriate course of action?

Extensive smoking hx and evidence of COPD and digital clubbing on PE- associates wrist pain with data entry but may be a sign of underlying lung disease. Hypertrophic osteoarthropathy (HOA) is a conditino where dig clubbing is accompanied by sudden onset arthropathy, commmonly affecting the wrist and hand joints. Hypertrophic pulmonary osteoarthropathy (HPOA) is a subset of HOA where the clubbing and arthropathy are attributable to underlying lung disease like lung cancer, tuberculosis, bronchiectasis, or emphysema. Given this patient's smoking history, lung cancer should be of particular concern. CXR is the most appropriate initial study for idenifying the underlying cause of his suspected HPOA.

Evaluation of a patient with dizziness

First step- classify as vertigo, presyncope or disequilibrium. Severe spinning sensation with nausea = vertigo. then classify as peripheral or central. Peripheral lasts for shorter intervals, 1-2 hrs is indeterminate. Ear fullness and preference for the other ear suggest a peripheral cause. Ear fullness is particularly suggestive of MENIERE'S disease, results form an abnormal accumulation of endolymph within the inner ear. The underlying etiology of Meniere's disease is not completely understood. Patients with Meniere's disease will often complain of hearing loss and tinnitus as well, which may be the reason this patient prefers to use her cell phone in the left ear.

26 year old white female to ER with severe sob. long hx of asthma/periodic exacerbation. Taking inhaled albuterol, steroid, salmeterol and cromolyn. Temp 99. BP 150/90, pulse 110/min, resp 24/min. On exam, she has moderate resp distress, prolonged exp phase, significant wheezing all over lung fields. Pt is admitted and given nebulized albuterol, iv steroids and o2. next day her resp status improved. vital signs normalized, labs: H 14, MCV 95, Leuk ct 19,000, seg neut 82%, bnads 3%, lympho 13%, eos/bas 0%, monocytes 2%. CXR normal except hyperinflated lungs. What is the most probable cause of the abnormal lab findings in this pt?

Most probable cause of leukocytosis in this patient is glucocorticoid-induced neutrophilia. Glucocorticoids have a complex effect on the blood cells. They tend to diminish the number of circulating eosinophils and have distinct lymphopenic effect. They also increase the neutrophil count by increasing the bone marrow release and mobilizing the marginated neutrophil pool. It is not uncommon to see neutrophilia during tx with glucocorticoids.

15/M 1 week hx of fever, non-productive cough, sore throat and headaches. Today he noticed a skin rash. His temp is 101.3. Throat is hyperemic, no cervical lymphadenopathy. Chest auscultation adn percussion > no abn. Dusky red, target shaped skin lesion over all 4 extremities. CXR reveals interstitial infiltrates in the left lower lobe. Sputum gram stain - polymorphonuclear cells but no organisms. Which organism is most likely responsible?

Mycoplasma pneumoniae -Atypical pneumonia causes: mycoplasma p, chlamydia p, legionella, coxiella, and influenza. MP is the msot common cause of atypical pna in the ambulatory setting. Atypical pna is sistinguished from pyogenic pna by its more indolent course, nonproductive cough, and higher incidence of extrapulmonary sx. Patient's low grade fever and week's worth of sx are consisten. Also the multiple extrapulmonary sx including headache, sore throat, skin rash. Erythema multiforme is typical of mycoplasma- an orgasm that does not have a cell wall and therefore does not stain with gram stain, hence the finding of only polymorphonuclear cells on sputum gram stain analysis.

27/M cough, chest discomfort, dyspnea on exertion, lost 10 pounds over 2 mos. Smoking 1 pack per day x 10 years. Drinks 2 beers every weekend. Denies illegal drug use, no multiple sexual partners. PE unremarkable. CXR reveals large anterior mediastinal mass. Blood shows elevated levels of HCG adn alpha fetoprotein. Most likely diagnosis?

Nonseminomatous germ cell tumor. Large anterior mediastinal mass with elevated levels of HCG and AFP - diagnostic of a germ cell tumor of the mediastinum. Primary mediastinal germ cell tumors occur in young males and are locally invasive. Beta hcg is typically elevated in both seminomatous and nonseminomatous germ cell tumors, but nonseminomatous germ cell tumors typically also produce alpha fetoprotein, which is not produced by seminomas. AFP and HCG elevations are indicative of a non-seminoma and therapy can be started even without a tissue biopsy.

65/F difficulty eating over last 2 days, food drops out of her mouth. Having discharge in left ear recently. Denies sore throat, nasal discharge, chest pain, cough or difficulty breathing. PMH sig for Type II DM, HTN, HLD. Ear canal shows granulations. There is facial asymmetry, and the angle of the mouth on the left is deviated downward. Which of the following is most likely the causitive organism?

Patient has Malignant otitis externa = severe infection seen in elderly diabetic patients that is most commonly caused by Pseudomonas aeruginosa. Patients typically present with ear pain and drainage that is not responsive to topical meds. The granulation tissue seen within the ear canal in this patient is a characteristic manifestation of MOE, and her hx of poorly controlled dm is a diagnostic clue. Progression of the infection can lead to food drop, as a result of damage to the left facial nerve. CT or MRI can be used to confirm the dx. Tx consists of systemic abx that are effective against Pseudomonas aeruginosa, such as Cipro. Tpical abx are ineffective.

37 year old woman presents to your office with severe vertigo, postural instability and vomiting. Also a buzzing sound in her right ear. Vitals WNL. Horizontal nystagmus found on PE> What could have prevented this patient's symptoms

Patient has Meniere's disease, which is a disorder resulting from distention of the endolymphatic compartment of the inner ear. The classic presentation consists of episodes of vertigo that last 20 mins to 24 hours in addition to low-frequency, sensorineural hearing loss and tinnitus. Vertigo can be accompanied by vomiting and postural instability. Sx typically wax and wane, but the course of the disease varies between individuals. Nystagmus may be seen during an acute attack, which is what this patient is currently experiencing. Triggers that increase endolymphatic retention should be avoided, including alcohol, caffeine, nicotine, and foods high in salt. A strict, salt-restricted diet of 2-3 grams of sodium per day is recommended as initial therapy, but hte evidence supporting its effects on controlling the sx of meniere's disease is not available. Medical therapy with diuretics, antihistamines, or anticholinergics is usually considered if lifestyle modifications are unsuccessful.

PE of CHF

Patients with worsening CHF will commonly have bibasilar crackles. Decreased breath sounds at the bases could be due to pleural effusions from CHF. Wheezing can occasionally be present in heart failure (cardiac asthma). Blood gas show hypoxia, hypocapnia and respiratory alkalosis- highly suggestive of CHF compared to COPD. Can cause tachypnea as left ventricular dysfunction allows fluid to pool in the lungs, causing a pleural effusion and hypoxemia due to reduced ventilation. Tachypnea causes hypocapnea and respiratory alkalosis. Exam typically shows signs of fluid overload, S3 and S4 gallops, cardiomegaly, and bibasilar crackles in the lungs

Pleural fluid: Characteristics of exudates: protein/serum ratio LDH/serum LDH ratio

Pleural fluid protein/serum protein ratio >0.5 Pleural fluid lactate dehydrogenase (LDH)/serum LDH ratio >0.6 Pleural fluid LDH > 2/3 of the upper limit of normal serum LDH Normal pleural fluid pH is approx 7.6. Transudative fluid is usually due to systemic factors eg increased hydrostatic pressure or hypoalbuminemia and has a pleural fluid pH of 7.4-7.55. Exudate is usually due to inflammation with a pleural fluid pH of 7.3-7.45. Pleural fluid pH < 7.3 with normal arterial pH and low pleural glucose) is usually due to increased acid production by pleural fluid cells and bacteria (eg empyema) or decreased hydrogen ion efflux from the pleural space. (Eg pleuritis, tumor, pleural fibrosis)

40 year old caucasian man comes to the ed b/c of fever, dry cough, and sob. Sx started 24 hrs ago. Denies hemoptysis. recently d/c from hosp after second cycle of chemo for AML. doesn't use tobacco, alcohol or drugs. Temp 102, bp 120/70, pulse 112, resp 28. Pt's pulse ox showed 86% at room air. Exam shows diffuse crackles all over the lung fields. CXR shows diffuse interstitial infiltrates. Which of the following is the most likely cause of his condition?

Pneumocystis jiroveci Pt is immunocompromised due to chemo, put him at risk for numerous opportunistic infections. Clinical presentation suggests atypical pna, along with characteristic CXR is suggestive of Pneumocystis jiroveci pna. P jiroveci is an opportunistic pathogen, an important cause of pna in immunocompromised hosts. Natural habitat is lung, incubation period ranges from 4-8 weeks. it is airborne transmitted. P jiroveci pna is characterized by dyspnea, fever, and nonproductive cough. PE would show tachypnea, tachycardia, and cyanosis with minimal chest findings. Bilat diffuse interstitial infiltrates beginning in the perihilar region is a characteristic finding on cxr in p jiroveci pna. P jiroveci may disseminate outside the lung, and the most common sites of extrapulmonary involvement are the lymph nodes, spleen, liver, and bone marrow.

38/M high grade fever, shaking chills, productive cough, SOB. 2 prior admissions for etoh withdrawal and seizures. Continues to drink. Temp 103.5. CXR demonstrates R lower lobe consolidation. Started on ceftiaxone and azithromycin. 12 hrs later, nurse says 38 RR. Emergent intubation is performed. what happened?

Pt admitted for PNA, he developed ARDS- often develops in the clinical setting of sepsis, pna, aspiration, toxic ingestions, trauma and/or burns. ETOHism is a further risk factor. Pathophys: release of inflammatory mediators as a result of local or distant tissue injury. These inflammatory mediators cause alveolar damage, increased alveolar capillary permeability, leakage of proteinaceous fluid into the alveoli. Clinically, leads to acute onset tachypnea, tachycardia, fever and dyspnea. ABG reveals hypoxemia and CXR reveals bilat alveolar infiltrates. Differential for hypoxemia and bilat infiltrates includes cardiogenic pulmonary edema. Pulmonary capillary wedge pressure <18 suggests ARDS**** while a value 18< suggests pulmonary edema. Dx criteria: acute onset of resp distress in the setting of a predisposing condition (sepsis, PNA, etc), PaO2/FiO2 ratio <200, bilateral infiltrates on CXR, normal PCWP.

Management of a patient with blunt abdominal trauma

Pt presenting with blunt abdominal trauma and/or shock should be assessed initially with a bedside abdominal ultrasound or FAST exam. IN hemodynamically unstable patients who have an equivocal or inconclusive FAST examination, diagnostic peritoneal lavage can accurate determine the presence of active intraperitoneal hemorrhage and subsequent need for emergency laparotomy

30/M with 3 day hx of fever, chills, sore throat. Difficulty swallowing. No cough/chest pain/difficulty breathing. Temp 102, voice is muffled, enlarged tender cervical lymph nodes on the left, uvula deviated to the right. Most appropriate treatment?

Pt's sx are secondary to a peritonsillar abscess. Although the 3-day hx of fever, chills, and sore throat were most likely secondary to tonsilitis, his muffled or "hot potato voice" and deviation of the uvula suggest that a peritonsillar abscess has developed as a complication of his tonsilitis. Patients with a peritonsillar abscess typically have prominent unilateral lymphadenopathy as seen in this pt. This condition can be fatal secondary to either airway obstruction or spread of the infection into the parapharyngeal space, which may lead to involvement of the carotid sheath. Initial tx consists of aspiration of the peritonsillar abscess adn initiation of intravenous abx. Surgical intervention may be necessary if the purulent material can't be removed with aspiration alone.

Common causes of hemoptysis

Pulmonary: bronchitis, pulmonary E, bronchiectasis, lung cancer Cardiac: mitral stenosis/acute pulmonary edema Infectious: TB, lung abscess Hematologic: coagulopathy vascular: arteriovenous malformations systemic diseases: wegener's granulomatosis, goodpasture's syndrome, SLE, vasculitis Pulmonary airway disease = most common cause: chronic bronchitis, bronchogenic carcinoma, bronchiectasis Bronchiectasis is more likely associated with a history of recurrent respiratory tract infections, chronic cough with copious mucopurulent sputum. Crackles, ronchi, wheezing are common.

29/F chest pain and exertional dyspnea x 10 d. PMH NSVD x 3 mos ago, after which she's had frequent episodes of dark bloody vag discharge. Most recent bleeding episode was 6 days ago. Patient denies fever, chills, hemoptysis, orthopnea or leg pain. Doesn't smoke cigarettes, drink alcohol, or use illicit drugs. Temp 99.5, pulse 80, bp 110/68, resp 16. Exam shows clear lungs. Pelvic shows enlarged uterus. CBC/serum electrolytes are all WNL. Chest rads show multiple bilateral infiltrates of various shapes. What investigation will be most helpful in establishing the diagnosis?

Quantitative beta HCG Choriocarcinoma is a form of gestational trophoblastic disease (GTD) that may occur after a normal gestation (25% of cases), molar pregnancy (50%), or abortion (25%). All forms of GTD tend to present with irregular vaginal bleeding, an enlarged uterus, and pelvic pain. Irregular vaginal bleeding beyond 8 weeks post-partum is abnormal and should raise suspicion for GTD. Malignant forms of GTD include invasive gestational trophoblastic neoplasia (GTN) and choriocarcinoma. While either may arise after a normal pregnancy, GTN is almost always only locally invasive while choriocarcinoma is highly metastatic. The most frequent site of metastatic spread in choriocarcinoma is to the lungs. This young woman's pulmonary symptoms (chest pain and dyspnea) are consistent with this diagnosis. Hemoptysis is also common. Obtaining a quantitative beta HCG is the appropriate next step in confirming the diagnosis. Suspect choriocarcinoma in any postpartum woman with pulmonary symptoms and multiple nodules on chest x ray. An elevated beta hCG helps to confirm the diagnosis.

32/F persistent cough and sob. had 3 episodes of pna over the last year. Severe sinusitis one year ago and an episode of bloody diarrhea that req hosp and iv abx therapy6 mos ago. doesn't smoke or drink. no drugs. no meds. All immunizations are up to date. BP 130/80, hr 90/min. PE: fine crackles over right lower lung lobe. No lower extremity edema present. Neck palpation doesn't reveal any lymph node enlargement. CXR shows right lower lobe infiltrates and left upper lobe fibrosis. ECG reveals non specific ST and T wave changes. Best next step in mgmt of this pt

Quantitative measurement of serum Ig Levels. Hx of recurrent bac infxns that is highly suggestive of immunodeficiency with involvement of humoral immunity. Selective immunoglobulin deficiency that includes IgA and/or IgA subfractions is a possible dx. For ex: selective deficiency of IgG3 alone is more common in adult females and is associated with recurrent sinopulmonary as well as GI infxns. Food allergies and autoimmune diseases may also be present. IgA deficiency and common variable immunodeficiency are also possible. The latter may be associated with suppressed cell immunity and increased risk of malignancy. Quantitative measurement of serum immunoglobulin levels helps to establish the diagnosis. Recurrent bacterial infections in an adult patient may indicate a humoral immunity defect. Quantitative measurement of serum immunoglobulin levels helps to establish the diagnosis.

MOdified wells criteria

Score +3 points -clinical signs of dvt -alternate diagnosis less likely than PE Score +1.5 points -Previous PE or DVT -HR > 100 Recent surg (<3 weeks) or immobilzation (>3 days) Score +1 point -hemoptysis -cancer Total score for clinical probability <4 PE unlikely >4 PE likely

Treatment of malignant otitis externa

Severe pseudomonal infection of the external auditory canal. Most patients are elderly, and often have poorly controlled dm. Primary sx are severe ear pain and drainage, and pts usually have a fever, the otoscopic finding of granulation tissue in the external auditory canal is consistent with MOE. OSteomyelitis of the skull base or TMJ can develop as the infection progresses, and may be in its early stages in this patient given her history of pain that is exacerbated with chewing. Involvement of the CN is sometimes seen as well. Given the severity of MOE, systemic therapy with an anti-pseudomonal antibiotic is recommended, with cipro IV being the drug of choice.

34/M rushed to the ED with SOB and difficulty swallowing. Agitated and gasping for breath. Prior visits for difficulty breathing, food intolerances and skin allergies. PE is notable for excessive accessory resp muscle use, retraction of the subclavicular fossae during inspiration, and scattered urticaria over the upper body. What is the most likely cause of his breathing difficulty?

Upper airway obstruction Patient with dyspnea, difficulty swallowing and physical findings suggestive of upper respiratory obstruction. Hx of food allergies and urticaria- laryngeal edema is likely the cause of his resp sx. Pts with laryngeal edema typically present with acute onset dyspnea. There's usually an identifiable precipitating event, eg peanut allery/etc. PE may reveal stridor and harsh respiratory sounds from trachea. Wheezing is generally absent on lung auscultation.

Mechanical ventilation and acid base response

While being mechanically ventilated, the patient is vulnerable to forced hyper-or hypoventilation. Ventilation is defined as the tidal volume multiplied by the respiratory rate. Hyperventilation (caused by increased tidal volume and/or resp rate) results in excessive CO2 losses and respiratory alkalosis, while hypoventilation (caused by decreased tidal volume and/or respiratory rate) results in CO2 retention and respiratory acidosis. The patient described is experiencing respiratory alkalosis as evidenced by his increased arterial blood pH (normal = 7.4) and his decreased PaCO2 (normal = 40 mm Hg). His serum bicarb level is decreased due to attempted renal compensation for the respiratory alkalosis. Specifically, the kidneys retain increased amounts of H+ (protons) an d excrete increased amts of bicarb in an attempt to normalize the serum pH. The increased amount of HCO3 in the urine alkalinizes the urine.

Mobile cavitary mass in the lung which presents with intermittent hemoptysis

aspergilloma- coarse fragmented septae, hyphae are typically seen. CXR may demonstrate a crescent radiolucency next to a rounded mass. Cavitary lesions may form because of destruction of the underlying pulmonary parenchyma, and debris and hyphae may coalesce and form a fungus ball, which lies free in the cavity and moves around with position change. Prophylactic resection is controversial, though some recommend resection if isolated disease is present in good risk patients.

blunt thoracic trauma, respiratory distress despite bilateral chest tubes

concerning for flail chest flail chest is usually due to a crush injury (steering wheel) causing more than 3 adjacent rib fractures that break in 2 places. This leads to an unstable chest wall segment that moves in a paradoxical motion with resp. The flail segment tends to retract inward during insp instead of normally bulging outward and bulges out during exp instead of normally retracting inward. Patients with flail chest present with rds and tachypnea with shallow breaths. however, muscle splinting with recruitment of chest wall muscles can mask the motion of the involved ribs and make it difficult to clinically detect an early flail segment. In addition, positive rpessure ventilation minimizes paradoxical wall motion. Pain control and supplemental oxygen are early steps in managmenet. Intubation with mechanical positive pressure vent is req in severe cases. People with multiple rib fractures are at risk for pulmonary contusions, which can lead to pna and acute rds.

25/M ed with sob and cough productive of blood tinged sputum x past few days. no fever, arthralgias or weight loss. never had sx before, no hx of recent travel or sick contacts. smokes 1/2 pack cigs daily, has had 2 sexual partners in 6 mos. On PE, temp 98.9, bp 120/70, pulse 102, resp 22. lungs reveal patchy bilateral rales, cxr demonstrates bilateral pulmonary infiltrates. serum cr is 2.6mg/dL and UA shows dysmorphic red cells. cause of current condition?

goodpasture's disease, a condition most common in young adult males. Renal findings include nephritic-range proteinuria (<1.5 g/d), acute renal failure, and urinary sediment with dysmorphic red cells and red cell casts. Pulmonary findings include SOB, cough, hemoptysis caused by pulmonary hemorrhage, systemic sx (fever, wt loss, arthralgias) are uncommon. the underlying cause is formation of antibodies to the alpha-3 chain of type IV collagen, a protein expressed most strongly in the glomerular and alveolar basement membranes. renal biopsy demonstrating linear IgG deposition along glomerular basement membrane on immunofluorescence is diagnostic.

aids and pna

pneumocystis jiroveci- hypoxia in pts with pna occurs secondary to alveolar and interstitial inflammation which causes areas of V/Q mismatch. This manifests as an increase in the A-a gradient.

Sensorineural hearing loss that occurs with aging

presbycusis- defined as sensorineural hearing loss that occurs with aging. Typically noticed in the 6th decade of life, characteristically begins with symmetrical, high frequency hearing impairment. Pts complain of difficulty hearing in crowded or noisy environments, difficulty hearing high-pitched noises or voices. Medications, genetics, hx of infection and exposure to loud noise affect this. Otosclerosis- chronic conductive hearing loss associated with bony overgrowth of the stapes. Typically begins with low-freq hearing loss and is often found in middle-aged individuals.

Approach to pt with suspected PE

Sudden onset of pleuritic chest pain, dyspnea, tachypnea, tachycardia and hypoxemia after a period of prolonged immobilization in this pt is highly suggestive of acute PE. First step in eval is supportive care with o2 for hypoxia and iv fluids for hypotension. next step assess for contraindications for anticoag. Pts with contra should undergo diagnostic eval for PE with appropriate tx: eg ivc filter, if positive. Pts without contraindications can be assessed with modified wells criteria for PE pretest probability. Dx testing is done before considering anticoag in pt with unlikely pe, however anticoag (eg lmwh or unfrac hep) should be given PRIOR to dx testing in pts with likely pe. Anticoag prevents further clots but doesn't lyse the existing clot. Dx eval usually involves CT angiogram of the chest in pts with normal renal fxn without contrast allergy. V/Q scan is an alternate imaging study for those with significant renal impairment/contrast allergy. Pts with positive dx test should continue anticoag and be considered for surgical thrombolectomy or thrombolytics if they are clinically unstable. Acute PE is asso with a mortality rate of ~30%, with recurrent PE the most common cause of death. Early and effective anticoag decreases the mortality risk with acute PE about 2-8%. Early empiric anticoag should be initiated prior to pursuing confirmatory dx testing in pts with high clinical suspicion of acute PE.

Patient with sever obesity and alveolar hypoventilation during wakefulness

Taken together, these findings point to a dx of Obesity Hypoventilation syndrome (OHS), aka pickwickian syndrome. Pts with OHS classically demonstrate extreme obesity (BMI = 55), a thick neck and hypersomnolence. Pt's distant heart sounds, low voltage QRS complexes on EKG, adn poor quality cxr are all findings consistent with obesity. This patient also has polycythemia secondary to alveolar hypoventilation, another common finding in OHS. The leg edema is noted on PE may be a sign of heart failure. Patient's ABG reveals resp acidosis, hypercapnea, hypoxemia. In OHS, derangement of the ABG is usually a consequence of decreased chest wall compliance which leads to increased work of breathing. Eventually, the work of breathing becomes so high that the CNS chemoreceptors establish a higher pCO2 set point, causing resultant hypoventilation, hypercapnia and hypoxemia. Respiratory muscle weakness also occurs in many OHS patients, but it is not the major cause of the clinical findings. Weight loss, ventilator support, O2 therapy, and progestins (a resp stimulant) are all potential therapies

35/M MVA, chest trauma. 800cc blood evacuated from chest, and 10 days later d/c home. Returns again with a low grade fever, dyspnea. CT scan reveals a complex loculated effusion with a thick surrounding peel. chest tube is placed, but after 24h, there is little drainage and the pt continues to have low grade fever. next step?

surgery empyema is an infection in the pleural space. can occur from parapneumonic effusions. Can also occur as a result of contamination of the pleural space by rupture of a lung abscess, a bronchopleural fistula, penetrating trauma, a thoracotomy, and infection from a hepatic or subphrenic abscess, or from a ruptured viscus (esophagus). common cause is hemothorax. residual blood in chest is an excellent medium for growth of bacteria. the indiv will usually present with low-grade fever, and empyema is best diagnosed with a CT scan. When the empyema is localized, complex, and has a thick rim, only sx is the ansewr. in surgery, the thick pleural peel is removed, the pus is removed and chest is drained. all old blood clots are drained and removed. Occurs most commonly due to bacterial seeding of parapneumonic effusion in the setting of bacterial pneumonia. Bacterial causes mirror those that cause pneumonia, namely strep pneumo, staph aureus and klebsiella pneumonia. A mixed aerobic/anaerobic bac population supersedes as the infected pleural effusion progresses to empyema- one of the reasons why empyema is often unresponsive to antibiotics normally used to treat CAP. Pts with empyema present with fever, cough (nonproductive or productive), sob and frequently pleuritic chest pain. Radiographic findings include a free-flowing (eraly) or loculated (late) pleural effusion and lung consolidation with air bronchograms. As in this patient, the effusion (opacity) typically has an abnormal contour. Tx requires drainage and abx.