Med

Front 1

First three steps in management of thunderclap headache.

Back 1

1. Non Contrast Head CT, if non-revealing:

2. Lumbar puncture, if non-revealing:

3. CT or MR Angiography

Front 2

Causes of a thunderclap headache?

Back 2

subarachnoid hemorrhage. Most of the other causes of thunderclap headache, such as an unruptured cerebral aneurysm, a carotid or vertebral artery dissection, cerebral venous sinus thrombosis, and reversible cerebral vasoconstriction syndrome

Front 3

First step in diagnosis of a possible peripheral polyneuropathy?

Back 3

EMG. Don't go for MRI first.

Front 4

stepwise spinal cord dysfunction without significant recovery and the MRI finding of a swollen spinal cord with dorsal flow voids. Dx?

Back 4

spinal dura-based arteriovenous fistula

Front 5

Medications that are contraindicated with myasthenia gravis?

Back 5

Ciprofloxacin and other fluoroquinolone medications are contraindicated in patients with myasthenia gravis; lithium, aminoglycosides, magnesium, and macrolide antibiotics.

Front 6

Patient presents with rapidly progressive neurologic disorder with weakness of limb, bulbar, and respiratory muscles. No sensory loss and normal DTRs. Dx? Test of choice? Tx?

Back 6

Given the absence of sensory loss and normal deep tendon reflexes, myasthenia gravis is the most likely diagnosis. Because of the rapid progression of the disease and the involvement of respiratory and bulbar muscles, the patient should be admitted to the hospital for management of a myasthenic crisis. Myasthenic crisis is a potentially life-threatening neurologic emergency characterized by weakness that is severe enough to necessitate intubation. Electromyographic studies, including repetitive stimulation of motor nerves, are indicated to establish a diagnosis of myasthenia gravis. Treatment of choice is plasma exchange.

Front 7

Young patient <age 40 comes in with Trigeminal Neuralgia. What is the first step.

Back 7

Trigeminal neuralgia in a patient this young should prompt evaluation for secondary causes, such as multiple sclerosis, posterior fossa tumors, and vascular or aneurysmal compression of the trigeminal nerve. (Don't treat first)

Front 8

Can central sleep apnea occur in asymptomatic LV dysfunction?

Back 8

Lanfranchi and colleagues (74) reported that 26 of 47 patients with asymptomatic LV systolic dysfunction (LVEF < 40%) had CSR-CSA.

Front 9

In Chf, do central and obstructive sleep apnea coexist?

Back 9

In a small minority of patients with HF, OSA and CSR-CSA coexist. In one study, Tkacova and colleagues (75) demonstrated that in such patients, there was a shift from predominantly OSA at the beginning of the night to predominantly CSA at the end of the night. This shift in apnea type occurred in association with a prolongation of lung to peripheral chemoreceptor circulation time, a lengthening of hyperpnea and a fall in PaCO2 from the beginning to the end of the night.

Front 10

What is the primary driver of ventilation during sleep?

Back 10

primary stimulation for ventilation while asleep is PaCO2. Central apnea during sleep occurs when PaCO2 falls below the apnea threshold. Patients with HF with CSR- CSA have lower PaCO2 than those without CSR-CSA in both the waking and sleeping states. Pulmonary congestion activates pulmonary vagal afferent C fibers, which stimulate central respiratory drive. Indeed, in patients with HF, PaCO2 is inversely proportional to pulmonary capillary wedge pressure. in patients with HF with CSR-CSA, PaCO2 tends not to increase from wakefulness to sleep (41, 42), but the apneic threshold does.

Front 11

What's the difference between cushings response and central sleep apnea associated hemodynamics?

Back 11

During central apnea, the absence of lung inflation deacti- vates pulmonary stretch receptors, and disinhibits central sym- pathetic nervous system outflow. As a consequence, blood pressure and heart rate oscillate in concert with Cheyne-Stokes cycles, very much as they do during OSA; peaks occur during hyperpneas and dips during apneas. Cushings response is widening pulse pressure, irregular breathing, and a reduction of the heart rate.

Front 12

Self resolving hemolytic anemia in a North African, Mediterranean, or middle eastern person

Back 12

Glucose 6 phosphate dehydrogenase deficiency. Enzyme levels may be normal in the setting of acute hemolysis because young erythrocytes have normal levels of the enzyme. Infectious, medication insult, of fava beans.

Front 13

What are the 6 clinical features of metformin toxicity?

Back 13

1. Type 2 diabetes or metformin use 2. Highly elevated lactate >15 3. Large anion gap >20 4. Severe acidemia pH <7.1 5. Very low bicarbonate <10 6. Hx of renal insufficiency, Cr >2.0

Front 14

When can you manage a spontaneous pneumothorax with observation?

Back 14

In the setting of secondary pneumothorax (known COPD), when there is less than 2cm between the chest wall and lung. Serial chest x rays and oxygen therapy.

Front 15

What are the most common risk factors for Amiodarone induced pulm toxicity?

Back 15

Increased age, dose, duration of therapy, preexisting lung disease.

Front 16

How can you distinguish between central and peripheral cyanosis? That is, blue blood that leaves the heart (central) vs blood that turns blue as it reaches the periphery?

Back 16

Peripheral cyanosis causes bluish discoloration of hands and feet, but the mucous membranes of the mouth are unaffected. Warming the patients limb skin often diminishes peripheral cyanosis because blood flow improves whereas central cyanosis stays the same or deepens. PaO2 will be low in central cyanosis but normal in peripheral cyanosis (you're sampling the arterial blood)

Front 17

You notice cyanosis of the mouth and lips and membranes, and you suspect central cyanosis. What's the next step and what does it help tell you?

Back 17

Administration of oxygen is the next step. If it fails to diminish the blue color, consider methemoglobinemia or sulfhemoglobibemia. Methemoglobinemia has a characteristic brownish hue.

Front 18

How can you tell if someone has pseudocyanosis?

Back 18

If lips are blue but mouth and membranes are normal. The bluish discoloration doesn't blanch with pressure on the skin. History of exposure to metals (argyia from silver; chrysiasis from gold) or drugs (Amiodarone, minocycline, chloroquine, or phenothiazines)

Front 19

What did the AMC randomized trial of CHOP versus rituximab-CHOP show in the treatment of AIDS related lymphoma?

Back 19

A significant increase in bacterial infection related deaths in those receiving rituximab plus CHOP at 14% versus 2% in the CHOP alone arm. Especially in those with CD4 counts less than or equal to 50.

Front 20

What are the two most common types of non Hodgkin lymphoma in AIDS? Which two subtypes of Hodgkin's disease are most common in AIDS?

Back 20

In NHL: burkitts and dlbcl In Hodgkin's disease: lymphocyte-depleted and mixed cellularity (both unfavorable subtypes)

Front 21

How does primary effusion lymphoma present?

Back 21

A lack of nodal disease with malignant effusions as the predominant feature

Front 22

Clinical features of Castleman disease?

Back 22

Polyclonal hypergammaglobulinemia, plasmacytosis, generalized lymphadenopathy, nodes containing perifollicular vascular proliferation, hepatosplenomegaly, constitutional symptoms. HHV8 (kaposi) thought to be involved.

Front 23

What physical exam finding is most sensitive and specific for the presence of anemia?

Back 23

Conjuctival rim pallor. Present if the inferior conjunctiva reveals the color of the anterior rim to have the same pale fleshy color of the deeper posterior aspect of the palpebral conjunctiva. No physical sign convincingly decreases the probability of anemia.

Front 24

Most common pathogens in bronchiectasis?

Back 24

H inf > P aer > Moraxella > Strep pneumo > staph > no organism > mycobacterium. King et al 2007 respir med 101: 1633

Front 25

What did the study of Tsang et al find in treatment of bronchiectasis exacerbation?

Back 25

35 bronchiectasis exacerbations most of whom had either H inf or pseudomonas and found no difference in clinical outcome in patients treated with either oral levofloxacin or Iv ceftazidime. Tsang et al Eur Respir J 1999; 14:1206

Front 26

What are the indications for surgery in bronchiectasis?

Back 26

Focal disease, do not respond to conventional therapy, uncontrolled hemoptysis despite interventional radiology techniques

Front 27

Focal bronchiectasis is found on high res ct of chest, what's the next step?

Back 27

Bronchoscopy. Evaluate local airway obstruction.

Front 28

A patient with pneumonia is found to have bronchiectasis on ct scan, what's the next step?

Back 28

Rarely acute pneumonia can result in "pseudobronchiectasis" so patients need to undergo a high res ct scan when clinically stable.

Front 29

High res ct of chest reveals diffuse bronchiectasis, what's the next step? Reveals right middle lobe bronchiectasis, what's the next step?

Back 29

Patients with diffuse bronchiectasis should be assessed for underlying systemic abnormalities including congenital abnormalities and immune mediated dysfunction. Right middle lobe and lingular predominant bronchiectasis with atypical mycobacterium.

Front 30

In acetaminophen overdose what comes first liver injury or renal injury?

Back 30

Renal injury, oliguria, and acute renal failure are seen in acetaminophen overdose although less common. Maximum renal injury lags beyond peak liver injury, and recovery is also more protracted. Isolated nephrotoxicity without hepatic injury rarely occurs. Renal failure may also be seen with FHF and hepatorenal syndrome

Front 31

The patient is admitted with acetaminophen overdose and they develop altered mental status, what is the next step in management?

Back 31

The mental status is typically clear after an acetaminophen overdose unless altered by a co ingested centrally active drug. However massive acetaminophen overdose may result in coma.

Front 32

What is the significance of metabolic acidosis in acetaminophen overdose?

Back 32

Metabolic acidosis is another uncommon finding early in the course of acetaminophen poisoning. The early metabolic acidosis may be a lactic acidosis or very rarely caused by a product of the gamma glutamate cycle 5-oxo proline. Lactic acidosis also occurs late secondary to hepatic failure with an inability to clear lactate.

Front 33

What are the statistics for the benefit of NAC when administered appropriately?

Back 33

NAC dramatically reduces the incidence of hepatotoxicity and progression to FHF when administered within the first 8 to 10 hours following acute overdose. In patients who received NAC within the first eight hours after overdose the risk of hepatotoxicity is less than 5% whereas delay beyond 10 hours is associated with an increased risk of hepatic injury

Front 34

What did the Keays paper BMJ 1991; intravenous acetylcysteine and paracetamol induced fulminant hepatic failure trial show?

Back 34

50 consecutive patients aged 16 to 60 with fulminant hepatic failure after paracetamol overdose who had not previously received acetylcysteine. Intervention, conventional intensive liver care plus either acetylcysteine in the same dose regimen as used early after a paracetamol overdose, except that the infusion was continued until recovery from encephalopathy or death, or an equivalent volume of 5% dextrose. Results, the rate of survival was significantly higher in the acetylcysteine treated group then in the controls 48% versus 20%. Acetylcysteine treated patients had a lower incidence of cerebral edema 40% versus 68% and fewer developed hypotension requiring inotropic support. However, rates of deterioration and recovery of liver function, were similar in the two groups.

Front 35

What are the risks of NAC?

Back 35

NAC induces the release of histamine from basophils and mast cells and in an in vitro model higher acetaminophen concentrations reduce the extent of NAC induced histamine release. A study by Waring and colleagues found a rate of anaphylactoid reactions of more than 20% of patients with an initial acetaminophen level 150 µg/ml whereas the incidence in patients with a level more than 200 µg/ml was less than 5%. Asthmatics may be at greater risk with IV NAC. Status asthmaticus with cardiac arrest and brain injury was reported in a patient with steroid dependent asthma during the loading dose of NAC.

Front 36

What are the contraindications to activated charcoal?

Back 36

Depressed level of consciousness, aspiration, uncontrolled vomiting, coingestion of a corrosive or proconvulsant. Activated charcoal does not significantly interfere with the efficacy of oral NAC.

Front 37

How do the majority of patients with systemic age-related non-Hodgkin's lymphoma present? How do patients in the HAART era likely present?

Back 37

Age-related non-Hodgkin's lymphoma presents with advanced stage disease and B symptoms. Extranodal disease bone marrow involvement and leptomeningeal disease are all common features. Patients in the HAART era are less likely to have had prior AIDS diagnosis, were older, and have higher CD4 cell counts at the time of diagnosis.

Front 38

How do you make the diagnosis of Amiodarone induced thyrotoxicosis?

Back 38

Significant previous Amiodarone use greater than four weeks not necessarily continuing at diagnosis (t1/2=100d) , hyperthyroidism including a raised free T4 level and a suppressed TSH level, clinical signs of hyperthyroidism, reduced thyroid radioisotope uptake and a negative anti-TSH receptor antibody.

Front 39

Which clinical and laboratory features can distinguish Amiodarone induced thyrotoxicosis from Graves' disease and toxic multinodular quarter?

Back 39

Amiodarone induced thyrotoxicosis occurs predominantly in elderly (68+/- 1.5) years of age, and male sex. Free T4 levels on average are significantly higher in AIT (45 pmol/l) similar to that seen in Graves' disease (45) but lower in toxic MNG (31). The free T4 to free T-3 ratio was increased in AIT (7.5) compared with graves and toxic MNG (3.1). Reduced conversion of T4 to T3 seen in Amiodarone thyroid dysfunction.

Front 40

What are the most significant predictors of death and amiodarone induced thyrotoxicosis?

Back 40

Severe left ventricular dysfunction, with an EF less than 30%, and age were significant predictors of death. Free T4, free T-3, cumulative Amiodarone dose and sex were not predictors. As long as t4 was elevated it did not matter how high it meant that there was a risk of death.

Front 41

What are the different forms of amiodarone induced thyrotoxicosis? How do the treatments differ?

Back 41

Type 1: excess iodine induced thyroid hormone synthesis in an abnormal gland (*increased vascularity on ultrasound, nml RAIU). Type two: destructive thyroiditis (absent hypervascularity, <3% RAIU). Type 1 AIT usually occurs in patients with pre-existing nodular goiter or latent Graves' disease, whereas type 2 generally develops in patients without clinical biochemical and morphological evidence of thyroid disease.

Front 42

How are the different forms of amiodarone induced thyrotoxicosis treated?

Back 42

Type 1 can be treated with methimazole 40-60 mg per day plus perchlorate <=1g/day, observing normalization of T3 on average by four weeks. In contrast, type 2 responds to 40 mg per day (0.5-0.7 mg per kg) of prednisone. Steroids and thionamides can be mixed. Resistant patients can be treated with iopanoic acid or surgery.

Front 43

Three clinical signs of hypovolemia? Three signs of euvolemia?

Back 43

Hypovolemia: abnormal skin turgor in subclavicular area (failed relaxation in 3sec), dry mucous membranes, dry axilla. Hypovolemia less likely with normal skin turgor and absence of tongue furrows.

Front 44

What is the class 1 indications for cardiac pacing in sick sinus syndrome?

Back 44

Sinus-node dysfunction with documented symptomatic bradycardia; possibly a consequence of necessary long- term drug therapy.

Front 45

What are the class 2 indications for pacemaker in sick sinus syndrome?

Back 45

Sinus-node dysfunction with heart rates <40 bpm; no clear association between symptoms and bradycardia

Front 46

What are the class 1 indications for pacemaker in AV block?

Back 46

Symptomatic complete or second-degree AV block, asymptomatic complete heart block with heart rates <=40 bpm, or consequence of His-bundle ablation

Front 47

Class 2 indications for pacemaker in AV block?

Back 47

Asymptomatic second-degree type II or complete heart block with heart rates >40 bpm

Front 48

Class 3 indications for pacemaker in AV block?

Back 48

First-degree AV block or asymptomatic second-degree type I AV block. class III, all conditions for which it is generally agreed that permanent pacing is not required

Front 49

Class 1 indications for pacemaker in bifasicular block?

Back 49

Fascicular block with intermittent complete heart block associated with symptoms or second-degree type II block with or without symptoms

Front 50

Class 2 indications for pacemaker in bifasicular block?

Back 50

HV intervals >100 msec (on ep study) or fascicular block associated with syncope that cannot be ascribed to other causes

Front 51

Class 3 indications for pacemaker in bifasicular block?

Back 51

Asymptomatic fascicular block or fascicular block with associated first-degree AV-node block

Front 52

Class 1 indications for pacemaker in neurogenic syncope?

Back 52

Recurrent syncope provoked by carotid-sinus stimula- tion; pauses of >3 seconds induced by minimal carotid-sinus pressure

Front 53

Class 2 indications for pacemaker in neurogenic syncope?

Back 53

Syncope associated with bradycardia reproduced by head-up tilting

Front 54

Class 3 indications for pacemaker in neurogenic syncope?

Back 54

Recurrent syncope in the absence of a cardioinhibitory response

Front 55

Class 1 or 2 indications for pacemaker in cardiomyopathy?

Back 55

Recurrent syncope in the absence of a cardioinhibitory response. No class 1 indications at this time.

Front 56

Class 3 indications for pacemaker in cardiomyopathy?

Back 56

Severely symptomatic patients with dilated cardiomyop- athy (may become class II in the future).

Front 57

Pathophysiology of vasovagal syncope

Back 57

result in part from the activation of myocardial mechano- receptors, leading to inhibited efferent sympathetic tone and increased efferent parasympathetic tone, which in turn result in peripheral vasodilatation and inappropri- ate bradycardia. Cardiac pacing may be beneficial in patients with marked bradycardia or ventricular asys- tole.

Front 58

What's better for cardiac pacing modes, Atrioventricular or solely ventricular pacing?

Back 58

Numerous studies have demonstrated better short- term and long-term hemodynamic improvement with atrioventricular synchronous pacing than with ventric- ular pacing, especially in patients at rest, but also to a variable extent during exercise.25-29 Atrioventricular synchrony allows efficient filling of the left ventricle, with up to 20 percent augmentation of end-diastolic volume and stroke volume.

Front 59

Clinical presentation of alveolar hemorrhage?

Back 59

mild haemoptysis, pulmonary infiltrates, and anaemia

Front 60

Most common causes of massive hemoptysis?

Back 60

Chronic inflammatory conditions (including bronchiectasis, tuberculosis, lung abscess) and lung malignancies are the most common causes of massive haemoptysis

Front 61

concurrent development of haemoptysis and menstruation

Back 61

catamenial haemoptysis. Periodical hemoptysis in association with menses.

Front 62

haemoptysis and spontaneous pneumothorax in a woman of childbearing age with diffuse interstitial abnormalities

Back 62

lymphangioleiomyomatosis.

Front 63

saddle nose, rhinitis, or perforated nasal septum with hemoptysis.

Back 63

Wegeners granulomatosis.

Front 64

oral or genital ulceration, uveitis, cutaneous nodules, and pulmonary artery aneurysm

Back 64

Bechets disease. 30% annual mortality in pts with PA aneurysm.

Front 65

massive haemoptysis in a patient with a tracheostomy. What's the next step?

Back 65

development of a tracheal-arterial fistula, usually the innominate artery. The prompt application of anterior and downward pressure on the tracheal cannula and overinflation of the tracheostomy balloon may help to tamponade the bleeding vessel, and immediate surgical review should be requested. Deflation of the tracheostomy balloon and removal of the tracheal cannula should be performed in a controlled environment.

Front 66

Mortality rate of hemoptysis when bleeding is >1000cc/24 hrs.

Back 66

The mortality rate is 58% when the rate of blood loss exceeds 1000 ml/24 hours, compared with 9% if bleeding is less than 1000 ml/hour.

Front 67

Mortality rate of hemoptysis in presence of malignancy?

Back 67

mortality rate in patients with malignancy is 59%, which increases to 80% in the presence of a combination of malignant aetiology and a bleeding rate of more than 1000 ml/24 hours

Front 68

In fatal PE, how much time do you have?

Back 68

Two thirds of patients with fatal PE will die within one hour of presentation. anatomically massive PE will only account for one half of those deaths, with the remainder attributed to smaller submassive or recurrent emboli.

Front 69

What is the definition of major PE?

Back 69

any combination of embolus size and cardiopulmonary function that results in a hemodynamically significant event. MPE is defined by the clinical spectrum ranging from hypotension to car- diac arrest. Syncope most likely represents an inter- mediary position, as the failure to regain conscious- ness inevitably results in cardiac arrest and those patients who recover consciousness have a high incidence of hypotension.

Front 70

A large PE occurs suddenly in your patient, what factors go into the stress on the RV?

Back 70

Initially, the compensatory maintenance of CO is achieved by a combination of catecholamine-driven tachycardia and the utilization of the Frank-Starling preload reserve (the latter being responsible for RV dilata- tion). This increase in RV cavitary pressure and radius serves to significantly increase RV wall stress (wall stress = pressure x radius).

Front 71

What are the four etiologies of hypoxemia in pulmonary embolism?

Back 71

Hypoxemia has been attributed to an increase in alveolar dead space, right-to-left shunting, ventilation/perfusion (V ̇ /Q ̇ ) inequality, and a low mixed venous O2 level. The two latter mechanisms are proposed to account for the majority of observed hypoxia and hypocarbia before and after treatment.

Front 72

What is the mechanism of V/Q mismatch in pulmonary embolism?

Back 72

redistribution of blood flow away from the embolized area, resulting in overperfusion of the unembolized lung regions and atelectasis that initially develops distal to the embolic obstruction yet persists after early embolism dissolution and result- ant reperfusion. Atelectasis may arise from a loss of surfactant and alveolar hemorrhage or an "air shift" phenomenon as regional hypocarbia related to regional hypoperfusion induces bronchoconstriction, both of which are compounded by humoral mediators released from platelet-laden emboli.

Front 73

What are the signs and symptoms of major pulmonary embolism in patients with COPD?

Back 73

Patients with CPD can manifest similar findings (tachycardia, tachypnea) but commonly have complex presentations that may be dominated by their underlying disease.

Front 74

Your patient in the ICU has invasive monitors placed, what are the different hemodynamic monitors that you notice when they suddenly develop a PE? PA pressure, RAP, SVR, CO, PCWP

Back 74

an increase in RAP; an increase in PA pressure (PAP); a decrease in cardiac index; and an increase in SVR. The validity of PCWP measurements in patients with massive PE have been questioned because the pressure can be recorded in a vascular zone that is occluded - PCWP is unreliable.

Front 75

Do ECG changes in PE mean there is cardiac stress or ischemia?

Back 75

two reports utilizing early myocardial scintigraphy with MIBI and CPK enzyme assessment in patients with anterior T-wave changes have failed to demonstrate perfusion defects or enzyme leaks that are suggestive of ischemia. Yoshinaga T, Ikeda S, Nishimura E, et al. Int J Cardiol 1999; 72:65-72 Ferrari E, Imbert A, Darcourt J. Eur Heart J 1995; 16(suppl):269

Front 76

What is the effect of shock on mortality in PE?

Back 76

Uniformly, the presence of shock is associated with a threefold to sevenfold increase in mortality. It is important to recognize that hemodynamically stable patients who are not in shock but who have experienced massive or submassive PE have similar mortality rates.

Front 77

What are the echocardiographic features of acute PE that differentiate it from other causes of RV dilatation?

Back 77

Patients with cor pulmonale or recurrent PE characteristically have a hypertrophied RV with a thickness of >5.0 to 7.0 mm preservation of the normal inspiratory collapse of the IVC, and a minimal septal shift, whereas acute RV failure secondary to RV infarct or acute PE should not be accompanied by RV hypertrophy and is accompanied by a minimal collapse of the IVC with inspiration. A septal shift is more charac- teristic of acute PE. The maximal velocity of the TR jet is directly proportional to the peak systolic pressure gradient between the RV and RA (delta P = 4V^2) and can reliably be used to estimate PAP.

Front 78

What is the average TR jet velocity in patients with acute PE? How can it differentiate other causes of RV strain? What is the relationship between TR jet velocity and PA pressure?

Back 78

The hypertrophied RV in patients with cor pulmonale or recurrent PE can generate a substantial PAP, occasionally approaching systemic pressures, and is associated with a TR jet of >3.5 to 3.7 m/s. RV infarct, cardiomyopathy, and dysplasia have impaired pressure-generating ability and a TR jet of < 2.5 to 2.8 m/s. Acute PE appears to be intermediate with a TR jet velocity of >2.5 to 2.8 m/s but <3.5 to 3.7m/s, which is consistent with the previous observations that a healthy ventricle cannot generate an mPAP of >40 mm Hg. The maximal velocity of the TR jet is directly proportional to the peak systolic pressure gradient between the RV and RA (delta P = 4V^2) and can reliably be used to estimate PAP.

Front 79

Your patient with suspected PE requires increasing oxygenation requirements and is intubated. He then develops worsened circulatory collapse and shock, what happened?

Back 79

First, sedative hypnotics used for intubation can blunt the catecholamine surge on which the patient is dependent for vasoconstriction as well as independently produce vasodilation, both of which impair hemodynamics the need for preload, catechol driven vasoconstriction and BP. Second, overzealous initial lung inflation can further decrease VR. Third, the initiation of mechanical ventilation can increase PVR, which can further decompensate the RV.

Front 80

Your patient with PE driven circulatory collapse is best intubated with which sedative agent?

Back 80

Etomidate is an ideal sedative because it preserves hemodynamic status.

Front 81

Your patient with a PE requires high amounts of heparin each day, >40,000 U/day. What do you do next?

Back 81

Suspect heparin resistance. When large doses of heparin are re- quired (ie, >40,000 U/d), the optimal heparin dose can be determined by antifactor Xa heparin levels.

Front 82

What is the difference between absolute risk reduction, relative risk reduction, and relative risk? What is the advantage of the use of each of them?

Back 82

Absolute risk reduction is defined as the difference between percentages. Percent mortality in the placebo group minus the risk of death in the treatment group. Verbalize it by using the population as the baseline: 6% of the population who took the drug had their life saved. The relative risk reduction is defined by the absolute risk reduction divided by the baseline risk of death in the placebo group. Verbalize it by using the drug as the baseline: the drug reduces the risk of death by 25%. The relative risk is defined as the ratio of percent mortality in the treatment group divided by percent mortality in the placebo group. Verbalize it by thinking of: the remainder of the risk in those who took the drug. Advantage of absolute risk reduction always places the benefit in terms of the population study. Relativist reduction transfers between populations despite any increase or decrease in the prevalence of outcome (In young populations who took aspirin the prevalence of death after MI is 4/1,000,000 but taking ASA still reduces the risk of death by 25% making the risk of death after taking the drug 3/1,000,000). RRR + RR = 1.

Front 83

What are the clinical manifestations of ABPA?

Back 83

Chronic asthma, recurrent pulmonary infiltrates, and bronchiectasis. hemoptysis, expectoration of brownish black mucus plugs, and history of pulmonary opacities in an asthmatic patient suggests ABPA

Front 84

What are the two clinical conditions that predispose to ABPA?

Back 84

about 1 to 2% in patients with asthma and 2 to 15% in patients with cystic fibrosis (CF)

Front 85

Describe the two types of aspergillus skin test.

Back 85

The reactions are classified as type I if a wheal and erythema developed within 1 min, reaches a maxi- mum after 10 to 20 min, and resolves within 1 to 2 h. A type III reaction is read after 6 h, and any amount of subcutaneous edema is considered a positive result. An immediate cutaneous hypersensitivity to A fumigatus antigens is a characteristic finding of ABPA and represents the presence A fumigatus- specific IgE antibodies, whereas a type III skin reaction probably represents the immune complex hypersensitivity reaction, although its exact signifi- cance remains unclear.

Front 86

How useful is serum IgE in ABPA?

Back 86

A normal serum IgE level excludes ABPA as the cause of the patient's current symptoms. The only situation where IgE levels can be normal in active ABPA is when the patient is already on glucocorticoid therapy.

Front 87

What are the most specific features of ABPA on imaging?

Back 87

High-attenuation mucoid impaction (mucus visually denser than the paraspinal muscle) is a pathognomonic finding encountered in patients with ABPA.23,90 -95 Central bronchiectasis with peripheral tapering of bronchi on HRCT is believed to be a sine qua non for the diagnosis of ABPA.

Front 88

Bronchiectasis is a pretty common finding in lung pathology, what features are specific to bronchiectasis in ABPA?

Back 88

bronchiectasis affecting three or more lobes, centrilobular nodules, and mucoid impaction are highly suggestive of ABPA.

Front 89

Name the major criteria for diagnosis of ABPA?

Back 89

Major criteria (mnemonic ARTEPICS) A = Asthma R = Roentgenographic fleeting pulmonary opacities T = Skin test positive for Aspergillus (type I reaction, immediate cutaneous hyperreactivity) E = Eosinophilia P = Precipitating antibodies (IgG) in serum I = IgE in serum elevated (> 1,000 IU/mL) C = Central bronchiectasis S =Serums A fumigatus-specific IgG and IgE (more than twice the value of pooled serum samples from patients with asthma who have Aspergillus hypersensitivity). The presence of six of eight major criteria makes the diagnosis almost certain; the disease is further classified as ABPA-S or ABPA-CB on the absence or presence of central bronchiectasis, respectively

Front 90

Itraconazole has been one of the therapies proposed for ABPA. What are its side effects and what interactions does it have with the other major treatment of ABPA?

Back 90

Monitor for adverse effects (eg, nausea, vomiting, diarrhea, and elevated liver enzymes). It also inhibits the metabolism of methylprednisolone (but not prednisolone) with resultant increased frequency of adrenal suppression.

Front 91

You call heme fellow overnight to discuss plasma exchange. She remarks that the patient needs a central line. What do you say in return?

Back 91

The Canadian Apheresis Study group found that 67% of 5234 TPE procedures could be completed successfully with peripheral venous access alone. Studies examining the complication rates of apheresis procedures have found that the frequency of complica- tions due to the placement of central venous catheters exceed the frequency of complications directly related to the procedure.24 In one study, all serious complications were related to central venous access, including a death due to a hemopneumothorax.

Front 92

What is therapeutic plasma exchange?

Back 92

TPE is a procedure in which a large volume of plasma is removed from a patient.2 The volume removed is such that if it were not replaced, significant hypovolemia resulting in vasomotor collapse would occur. As a result, the removed plasma must be replaced with some form of replacement fluid (albumin and saline).

Front 93

What are the treatment complications of IVIG?

Back 93

One formulation of IVIG contains significant amounts of sucrose, which can cause acute kidney injury. It is though that the sucrose causes swelling and vacuolization of the tubules. This risk is affected by the total dosage of IVIG, the rate of infusion, as well as risk factors pre-disposing a patient to acute kidney injury such as diabetes and decreased oral intake.

Front 94

Should we prophylactically anti coagulate patients in normal sinus rhythm who have systolic heart failure?

Back 94

In the 2012 WARCEF trial, Homma and colleages compared aspirin to coumadin in 2305 patients with heart failure. At 6 years follow-up, there was no significant difference in terms of ischemic stroke, ICH, or death.

Front 95

What are the common etiologies of hypercalcemia?

Back 95

Primary hyperparathyroidism and malignancy are the two most common causes of hypercalcemia. However, hyperthyroidism can also cause hypercalcemia. Although the mechanism is incompletely understood, T3 is thought to stimulate osteoclast differentiation by induction of IL6, RANK and prostaglandin, leading to accelerated bone resorption and subsequent hypercalcemia.

Front 96

What are the available tools to help make the diagnosis of interstitial cystitis?

Back 96

Interstitial cystitis is a frequent diagnosis in outpatient medicine. The OLeary-Sant Symptom and Problem Index is a questionnare that include urinary and pain symptoms to help physicians make the diagnosis of interstitial cystitis.

Front 97

Describe the results of the Colchicine in Addition to Conventional Therapy for Acute Pericarditis (COPE) Trial.

Back 97

- Colchine shows benefit primarily in preventing recurrence not necessarily in sx relief.
- Tx dose of NSAIDS is 800 TID
- steroids are only used in refractory pericarditis not responding to nsaids/colchicine or if they can't use the first line meds.

Front 98

Is there an association between clozapine and myocarditis?

Back 98

There is a well-described association between clozapine and and eosinophilic myocarditis, originally described between 1:10,000 and 1:1,000 and the mechanism is hypothesized to be an IgE-mediated hypersensitivity.

Front 99

Are the patients with thalassemia at an increased risk of infection?

Back 99

Infection is the number 2 cause of death (after cardiovascular disease) in patients with thalassemia, with 12% of patients with thalassemia major succumbing to infection. Increased susceptibility to infection is believed to be due to creating an iron rich environment for bacteria growth (i.e. Yersinia enterolitica).

Front 100

What are the symptoms of Lymphogranuloma venereum (LGV) and how is it treated?

Back 100

LGV is caused by C. trachomatic serovars L1, L2, L3 and initially presents with a painful genital ulcer, which progresses to painful lymphadenopathy. Recommended treatment is doxycycline 100mg orally twice daily for 21 days.

Front 101

Do patients with multiple cardiac risk factors need more intensive evaluation prior to starting exercise regimens?

Back 101

The AHA recommends physician medical clearance for all high risk patients, specifically those with three or more cardiac risk factors and those patients who have a history of myocardial infarction. Clearance is also recommended for patients with moderate cardiac risk factors undergoing vigorous activity.

Front 102

How would you dose epinephrine for anaphylaxis?

Back 102

Dosing of epinephrine for anaphylaxis is 0.2-0.5mg of 1:1,000 (1mg/ml) dilution IM or 0.1mg of 1:10,000 (0.1mg/ml) dilution IV. Therefore, 0.2-0.5cc of epinephrine 1:1,000 or 1cc epinephrine 1:10,000 should be given IM or IV, respectively.

Front 103

Which of the forms of malaria are dormant in the liver? Which cause severe malaria infection?

Back 103

Although the Plasmodium falciparum and knowlesi cause a severe malaria infection, P.vivax and ovale form dormant hypnozoites in the liver, requiring additional treatment with primaquine.

Front 104

Describe the risks and benefits and usual procedure for patients who need surgery and have coronary stents?

Back 104

Patients with coronary stents that are taking both aspirin and clopidogrel should defer surgery for at least 6 weeks after bare metal stent and 6 months after drug eluting stent placement. If the patient requires surgery within 6 weeks of BMS or within 6 months of DES placement, the patient should be continued on both aspirin and clopidogrel.

Front 105

Your patient is bradycardic and lightheaded and pre-syncopal, should you use atropine?

Back 105

It depends, first do an EKG. 1. Atropine should not be given in symptomatic bradycardia from complete heart block or type II Mobitz as these blocks are often infranodal and unlikely to respond to vagal blockade.

Front 106

Define the Lille score in Alcoholic hepatitis?

Back 106

In patients with alcoholic hepatitis, the Lille score assesses improvement after one week of treatment, with lower scores indicating a reduced mortality ([HR] 0.18, 95% CI 0.05-0.71).

Front 107

For which patients do you do a CT prior to LP?

Back 107

The following adults with suspected meningitis should undergo a CT prior to lumbar puncture: immunocompromised, history of CNS disease, new onset seizure, papilledema, abnormal level of consciousness, focal neurologic deficit.

Front 108

What is the age for initiation of Pap testing and HPV testing in women?

Back 108

Begin Pap at 21 years old q 3 years.
Co-testing for HPV should start at 30 years old and extends the screening interval to five years.

Front 109

What is the differential diagnosis of an anterior mediastinal mass?

Back 109

Terrible lymphoma, Teratoma, Thymoma, and Thyroid cancer.

Front 110

How soon should you initiate therapeutic hypothermia?

Back 110

There is a 20% increase in mortality for every hour of delay in the initiation of therapeutic hypothermia.

Front 111

What's the most accurate and helpful way to provide cooling to patients you want to induce therapeutic hypothermia in after ROSC is achieved? What the typical goals?

Back 111

Several liters of cooled IV saline will promptly decrease temperatures by 1 deg Celsius within 30 minutes, will help prevent post-ROSC hypotension, and can be delivered in the ER.

Front 112

In what temperature range does shivering most often occur in therapeutic hypothermia?

Back 112

Between 35 and 37 degrees celsius.

Front 113

What percentage of patients who have ROSC and undergo therapeutic hypothermia develop infections? What are the most common etiologies?

Back 113

More than 67% of patients who undergo therapeutic hypothermia develop infections. The most common being pulmonary infections from CPR, intubation, and ventilation contributing.

Front 114

When is it safe to start a biologic agent for psoriasis in a patient with latent tuberculosis?

Back 114

The recommendation from an expert panel of dermatologists state that for compliant and reliable patients, biologics can be start after one month of latent TB therapy.

Front 115

Is there a benefit to a clopidogrel "reload" in patients who present with acute coronary syndrome, are already taking clopidogrel?

Back 115

The ARMYDA-4 RELOAD trial looked at 503 patients (41% with NSTEMI) who randomly received 600mg of clopidogrel loading 4-8h before PCI (n=252) or placebo (n = 251) who were slated to undergo PCI. Primary endpoint was 30day incidence of major adverse cardiac events (MACE). Only patients with ACS had significant clinical benefit with reloading (6.4 vs 16.3%). There was no excess bleeding in the reload arm (6% in both groups.
Di Sciascio et al. Eur Heart J 2010; 31(11):1337-43

Front 116

In patients with non-small cell lung cancer, what are genotype-directed options for chemotherapy?

Back 116

For patients with NSCLC who are known to carry an EGFR mutation, the nationall comprehensive cancer network suggests erlotinib (Tarceva) monotherapy as first-line. The guidelines even reserve erlotinib as a salvage treatment option in this subgroup among patients with an ECOG performance status of 4 (completely disabled, totally confined to bed).

Front 117

What are the current guidelines for lung CA screening?

Back 117

USPSTF has issued a draft recommendation that physicians screen high-risk (30 cig-pack-years and who are still smoking or quit within the past 15 years) who are 55 to 79 yrs old for lung CA annually, using low-dose CT scans.

Front 118

What are the risks of thrombosis, and stroke in the peri-operative period in patients with AF and valves and prior VTE? What is their risk of bleeding?

Back 118

Overall rates (with and without bridging) are higher: 1.2% among patients with a mechanical heart valve, 0.9% among those with atrial fibrillation, and 1.8% among those with venous thromboembo- lism.44 Corresponding rates of major bleeding (with and without bridging) are 2.7%, 2.0%, and 1.9%, respectively.

Front 119

What mode of bridging would you use for a high risk (high CHADS2) patient with CrCl <30?

Back 119

When bridging therapy is required for high- risk patients with an estimated creatinine clear- ance of less than 30 ml per minute, the use of unfractionated heparin is preferred.

Front 120

What do you do for peri-procedure bridging therapy in a patient with low-risk of thrombosis?

Back 120

For low-risk patients, such as those with thromboembolism more than 3 months before the planned procedure, prophylactic low-dose heparin can be used for bridging.

Front 121

You have a patient undergoing an invasive procedure in a few weeks. You need to stop their warfarin, but when can you safely stop it and be sure that they will be at a safe level for the procedure?

Back 121

93% of patients with an INR 2-3.0 have an INR of less than 1.5 approximately 5 days after warfarin therapy has been discontinued

Front 122

Whats the half-life and duration of unfractionated heparin?

Back 122

Unfractionated heparin administered intravenously has a half-life of 60 to 90 minutes, and anticoagulant effects dissipate 3 to 4 hours after discontinuation. Thus, the infusion is stopped 4 to 6 hours before high-risk procedures.

Front 123

Does aspirin or dipyridamole increase the risk of clinically significant post-procedural bleeding?

Back 123

Aspirin and dipyri- damole individually do not substantially increase the risk of clinically important postprocedural bleeding but are sometimes discontinued before certain elective high-risk procedures. Adminis- tration of aspirin and dipyridamole together (i.e., Aggrenox [Boehringer Ingelheim]) probably increases the risk of postprocedural bleeding.

Front 124

Your patient is going to down for an IVC filter, why do you call the interventional radiologist does?

Back 124

The filter should be removable, whenever possible, because of the risks of long-term adverse events with permanent filters

Front 125

What are the indications for an IVC filter?

Back 125

Patient has proximal DVT in the legs and has one of the following conditions:
A contraindication to anticoagulation
Pulmonary embolism during anticoagulation
A free-floating thrombus (i.e. the leading edge of the thrombus is not adherent to the vessel wall)
Poor cardiopulmonary (heart) reserve and unlikely to tolerate a pulmonary embolus
Patient does NOT have proximal DVT in the legs but has one of the following conditions:

Requires long-term prophylaxis of pulmonary embolism (e.g. patients with a history of recurrent pulmonary embolism)
Has a high risk of thromboembolism and a high risk of of hemorrhage from anticoagulants drugs (e.g. trauma victims)
DVT/PE has occurred within the previous 4 weeks and an urgent procedure is required off anticoagulation In such cases, filters can prevent pulmonary embolic events and allow the temporary discontinuation of anticoagula- tion therapy.

"DVT can CPFH" - DVTs can cut people's feet in half. (Contra, Pulm Emb, Free-floating, Heart)
"No DVT can LH" - No DVT can launch heights. (Long term, high risk)

Front 126

What is the side effect of FFP that is most feared?

Back 126

The administration of fresh- frozen plasma may lead to volume overload in patients with advanced cardiac or kidney disease.

Front 127

When do you choose PCC over FFP?

Back 127

Prothrombin complex concentrates are preferred in cases of bleeding related to vitamin K antagonist treatment,49 particularly for patients with heart failure, valvular heart disease, or renal fail- ure, in whom a large-volume infusion of fresh- frozen plasma may result in volume overload.

Front 128

What factors are found in PCC?

Back 128

Non-activated 4-factor PCCs (Factors II, VII, IX, X and proteins C and S) have been preferred over plasma for severe warfarin-related bleeding and are effective with minimal volume. Kcentra, has just been FDA approved for urgent reversal of Vitamin K-induced coagulation deficiency and severe bleeding. An ''activated'' 4-factor PCC, Factor VIII Inhibitor Bypass Activity (FEIBA NF). Non-activated 3-factor PCCs (which contain factors II, IX, and X and only small amounts of factor VII) are available in the United States (Bebulin VH, and Profilnine SD)

Front 129

Which of the anti-Xa inhibitors are dialyzable?

Back 129

Unlike dabigatran (which is dialyzable), rivaroxaban and apixaban are not dialyzable.

Front 130

Which anti-platelet agents can you start within 24 hours after a moderate risk procedure? Which do you need to wait for 48 hrs?

Back 130

ASA and Clopidogrel can be started within 24 hours because of their delayed onset of action if hemostasis is achieved. Prasugrel or ticagrelor need to be delayed because of their rapid onset of action, potent antiplatelet inhibition, and the lack of agents to reverse their effects.

Front 131

Describe the trial recommending prasurgrel? What was the clinical benefit? What was the most serious side effect?

Back 131

TRITON-TIMI 38 randomly assigned 13,608 patients with moderate- to high-risk ACS, of whom 10,074 (74%) had UA/NSTEMI, to receive prasugrel (a 60-mg loading dose and a 10-mg daily maintenance dose) or clopidogrel (a 300-mg loading dose and a 75-mg daily maintenance dose). Prasugrel was associated with a significant 2.2% absolute reduction and a 19% relative reduction in the primary efficacy endpoint, a composite of the rate of death due to cardiovascular causes (including arrhythmia, congestive heart failure, shock, and sudden or unwitnessed death), nonfatal myocardial infarction (MI), or nonfatal stroke during the follow-up period. Rates of cardiovascular death (2.1% versus 2.4%; p=0.31) and nonfatal stroke (1.0% versus 1.0%; p=0.93) were not reduced by prasugrel relative to clopidogrel. Rates of stent thrombosis were significantly reduced from 2.4% to 1.1% (p<0.001) by prasugrel.
Prasugrel was associated with a significant increase in the rate of bleeding, notably TIMI (Thrombolysis In Myocardial Infarction) major hemorrhage, which was observed in 2.4% of patients taking prasugrel and in 1.8% of patients taking clopidogrel.

Front 132

What group of patients should prasurgel be avoided in?

Back 132

A post hoc analysis of TRITON-TIMI38 suggested there were 3 subgroups of ACS patients who did not have a favorable net clinical benefit (defined as the rate of death due to any cause, nonfatal MI, nonfatal stroke, or non-CABG-related nonfatal TIMI major bleeding) from the use of prasugrel or who had net harm: Patients with a history of stroke or transient ischemic attack before enrollment had net harm from prasugrel (HR: 1.54; 95% CI: 1.02 to 2.32; p􏰂0.04); patients 􏰈75 years of age had no net benefit from prasugrel (HR: 0.99; 95% CI: 0.81 to 1.21; p􏰂0.92); and patients with a body weight of 􏰁60 kg had no net benefit from prasugrel (HR: 1.03; 95% CI: 0.69 to 1.53; p􏰂0.89). In both treatment groups, patients with at least 1 of these risk factors had higher rates of bleeding than those without them

Front 133

When do you think about giving prasurgrel?

Back 133

Prasugrel was administered only after a decision to proceed to PCI was made. It is not our recom- mendation that prasugrel be administered routinely before angiography, such as in an emergency department, or be used in patients who have not undergone PCI.

Front 134

Among patients with chest pain, what are the features that are most suggestive of ACS?

Back 134

Among patients considered to have angina, there are three presentations of angina that suggest an acute coronary syndrome (ACS):

Rest angina, which is usually more than 20 minutes in duration
New onset angina that markedly limits physical activity
Increasing angina that is more frequent, longer in duration, or occurs with less exertion than previous angina.

Front 135

What goes into the TIMI calculation?

Back 135

Each of the following would get one point:
Age, >=65yo
At least 3 risk factors for CAD (family hx CAD, HTN, HLD, DM, or being a current smoker)
Significant coronary stenosis (eg, prior coronary stenosis >=50%)
ST deviation
Severe anginal symptoms (eg, >=2 anginal events in last 24 h)
Use of aspirin in last 7 days
Elevated serum cardiac markers (either CK-MB or Troponin)
If you don't know if the patient had Cath in the past or the results of cath, that's OK, you can leave it out and count it as zero - it has the same effect on average.

Antman EM, et. al. JAMA, August 16, 2000 PMID: 10938172

Front 136

Is dipyridamole recommended as anti-platelet therapy in UA/NSTEMI?

Back 136

Dipyridamole is not recommended as an antiplatelet agent in post-UA/NSTEMI patients because it has not been shown to be effective

Front 137

How is clopidogrel metabolized in the body?

Back 137

Clopidogrel is a prodrug and requires conversion to R130964, its active metabolite, through a 2-step process in the liver that involves several CYP450 isoenzymes (81); of these, the CYP2C19 isoenzyme is responsible for almost half of the first step formation (78). At least 3 major genetic polymorphisms of the CYP2C19 isoenzyme are associated with loss of function: CYP2C19*1, *2, and *3

Front 138

What did the CURRENT OASIS trial show?

Back 138

The CURRENT-OASIS trial randomized 25,086 patients with ACS who were intended for PCI and who were not considered to be at high risk for bleeding to receive higher-dose clopidogrel (600 mg loading, 150 mg daily for 6 days, 75 mg daily thereafter) versus standard-dose clopi- dogrel (300 mg loading, 75 mg daily) Although the overall trial (96) failed to demonstrate a significant difference in the primary endpoint between the clopidogrel and ASA groups (4.2% versus 4.4%), the primary outcome was reduced in the PCI subgroup random- ized to higher-dose clopidogrel (3.9% versus 4.5%; p􏰂0.035), and this was largely driven by a reduction in myocardial (re)infarction (2.0% versus 2.6%; p􏰂0.017).

Front 139

What did the EARLY ACS trial show?

Back 139

The EARLY ACS trial studied early routine administration of the GP IIb/IIIa inhibitor eptifibatide would be superior to delayed provisional administration. Early routine eptifibatide administration was associated with a greater risk of TIMI major hemorrhage (2.6% versus 1.8%; p􏰂0.02).

Front 140

What is a good marker of the probability of access site thrombosis in a patient with ESRD?

Back 140

probability of vascular access site thrombosis 12 months after insertion was 18.4% for arteriovenous fistulae and 39.9% for arteriovenous grafts, for patients with a serum albumin <30 g/L, and was 14.4% for fistulae and 32.3% for grafts for patients with a serum albumin >30 g/L

Front 141

What is the initial treatment of choice for DVT in ESRD patients?

Back 141

For the initial treatment of VTE, unfractionated heparin is preferred anticoagulant in patients with ESRD, and should be administered using a weight-based nomogram and continued for at least 5 to 7 days or until the INR is therapeutic for two consecutive days

Front 142

Your dialysis patient lacks vascular access and develops a DVT. What do you do for now?

Back 142

In patients without venous access, unfractionated heparin can be administered in a weight-adjusted, twice-daily subcutaneous dose, with mid-interval anticoagu- lant monitoring (aPTT) done 6 h after the prior heparin dose.

Front 143

Is there any difference between thrombolytics, device-based, or thrombectomy for thrombosis of vascular access site in HD patients?

Back 143

Kidney Diseases Outcomes Quality Initiative Working Group: This group found no clear evidence to recommend one method over another for the treatment of clotted grafts, where all of the techniques appear, in experienced hands, to lead to immediate patency rates around 85%.

Front 144

Your patient with AV fistula thrombosis develops a clot. Should you suspect another clot elsewhere?

Back 144

In either case, proximal stenosis often underlies the thrombosis and the treatment plan should include the evaluation and percutaneous or surgical management of the stenosis either as part of the original declotting procedure or as soon as possible afterwards.

Front 145

What is the risk of bleeding in patients with CKD on warfarin? Is there any benefit to giving low-dose warfarin?

Back 145

Low- and full-intensity anticoagulation use in HD patients is associated with a significant bleeding risk, which has to be balanced against any potential benefit of therapy. This has to be considered carefully when prescribing warfarin to HD patients.

Front 146

What is your goal anti-Xa level in patients on LMWH?

Back 146

in patients receiving twice-daily LMWH (e.g., enoxaparin 1 mg/kg BID), the target therapeutic anti-Xa level is 0.6—1.0 IU/mL; and in patients receiving once- daily LMWH (e.g., tinzaparin 175 IU/kg), the target therapeutic anti-Xa level is 1.0—2.0 IU/mL

Front 147

You are called to see a 67-year-old man with type 2 diabetes mellitus and end-stage renal failure secondary to diabetic nephropathy who presents with retrosternal chest pain and hypotension (blood pressure 85/60 mmHg) one h into his usual hemo- dialysis session. Despite receiving 2 doses of nitroglycerin 0.3 mg sublingually, the patient con- tinues to complain of chest pain, now ongoing for 20 min. Review of the patient's medical chart reveals a longstanding history of hypertension, dyslipidemia and a prior transient ischemic attack, with no prior history of cardiac disease or serious bleeding. You note that his dry weight is 85 kg. His current medications include aspirin, atorvastatin diltiazem and ramipril. On examination, he appears pale, with cool, clammy extremities. His blood pressure has increased to 95/70 mmHg after stopping hemodialysis, heart rate is 90 per min and regular respiratory rate is 25 per min and shallow, and he is afebrile. A 12-lead electrocar- diogram demonstrates 1—2 mm ST-segment depres- sion in the anterolateral leads. Cardiac troponin I levels are drawn, but are pending. You make a provisional diagnosis of an ACS. What are the options for antithrombotic management in this patient?

Back 147

Unfractionated heparin. An initial bolus of 60—70 U/kg (maximum 5000 U) and initial infusion of 12—15 U/ kg/h (maximum 1000 IU/h) titrated to a target activated partial thromboplastin time (aPTT) of 50—75 s is recommended

Front 148

What is the most accurate effect of protamine on LMWH?

Back 148

In comparison to unfractionated heparin, rever- sal of the LMWH anticoagulant effect is unpredict- able using protamine sulfate. Animal and in vitro studies have demonstrated that protamine neutra- lizes the antithrombin (anti-IIa) activity, but only 60% of the anti-factor Xa activity of LMWHs

Front 149

When should antithrombotic therapy be interrupted prior to interventional procedures in patients with renal insufficiency?

Back 149

The presence of renal insufficiency does not influence the timing of discontinuation of antith- rombotic therapies. Unfractionated heparin is usu- ally discontinued 6 h prior to interventional procedures, with an aPTT level drawn prior to the procedure to ensure no anticoagulant activity is present. For LMWHs, the dose immediately prior to the procedure is usually held; hence, when admin- istered on a twice-daily, or once-daily basis, a minimum of 12 or 24 h occurs between the last dose and procedure, respectively. Anti-Xa levels are not routinely measured prior to the procedure.

Front 150

Is there any known benefit from therapeutic hypothermia in patients for IN-HOSPITAL cardiac arrest?

Back 150

The only retrospective study that performed this was in selected hospitalized patients (n=118), WITHOUT terminal illnesses, which showed no difference in neurological outcome in patients that underwent therapeutic hypothermia.
Kory et. al. Neurocritical Care (2012) 16:406-412

Front 151

What is the definition of resistant hypertension?

Back 151

Resistant hypertension is defined as blood pressure that remains above goal in spite of the concurrent use of 3 antihypertensive agents of different classes.

Front 152

My patient requires 4 medications for hypertension, one of which is a diuretic and the rest are at max dosages. What's the next step?

Back 152

Although arbitrary in regard to the number of medications required, resistant hypertension is thus defined in order to identify patients who are at high risk of having reversible causes of hypertension and/or patients who, because of persistently high blood pressure levels, may benefit from special diagnostic and therapeutic considerations. As defined, resistant hypertension includes patients whose blood pressure is controlled with use of more than 3 medications. That is, patients whose blood pressure is controlled but require 4 or more medications to do so should be considered resistant to treatment.

Front 153

What's your goal BP in patients with CKD?

Back 153

<130/80

Front 154

In patients with resistant hypertension, what percentage is caused by secondary causes?

Back 154

Secondary causes of hypertension are common in patients with resistant hypertension, although the overall prevalence is un- known. It is important to keep in mind lifestyle factors however first.

Front 155

What are the lifestyle factors associated with resistant hypertension?

Back 155

Obesity, dietary salt (more than 10g in urine/24 hrs), ETOH (more than 30 drinks a week), NSAIDs, COX2, diet pills, stimulants, OCPs, Cyclosporine, Erythropoietin

Front 156

In what age group should we suspect secondary causes of hypertension?

Back 156

The likelihood of a readily definable second- ary cause of hypertension is greater in older patients because of a greater prevalence of sleep apnea, renal parenchymal disease, renal artery stenosis, and possibly primary aldosteronism.

Front 157

What clinical manifestations make you think of primary aldosteronism?

Back 157

In an evaluation of more than 600 patients with hypertension, the prevalence of primary hyperaldosteronism was found to be 6.1%. 56 In this study, the prevalence of primary aldosteronism varied according to the underlying severity of hypertension, with a prevalence of 13% among patients with severe hypertension (>180/110 mm Hg). Importantly from a clinical standpoint, in this study and others documenting a high prevalence of primary aldosteronism, serum potassium levels were rarely low in patients confirmed to have primary aldosteronism, suggesting that hypokalemia is a late manifestation of the disorder preceded by the development of hypertension.

Front 158

What causes primary aldosteronism?

Back 158

As in the general hypertensive population, the stimulus for the aldosterone excess in patients with resistant hyper- tension has not been identified. Preliminary results relate aldosterone excess to sleep apnea in patients with resistant hypertension, thus correlating it with the increasing incidence of obesity.

Front 159

When should you suspect pheochromocytoma?

Back 159

The diagnosis of pheochromocytoma should be enter- tained in a hypertensive patient with a combination of headaches, palpitations, and sweating, typically occurring in an episodic fashion, with a diagnostic specificity of 90%.

Front 160

What's the best screening test for pheochromocytoma?

Back 160

The best screening test for pheochromocytoma is plasma free metanephrines (normetanephrine and meta- nephrine), which carries a 99% sensitivity and an 89% specificity.

Front 161

What's the main mechanism for hypertension in Cushing's syndrome?

Back 161

The main mechanism of hypertension in Cushing's syndrome is overstimulation of the nonselective mineralocorticoid receptor by high cortisol levels.

Front 162

Your patient with CKD comes in for a BP visit. What's the pathophysiology that runs through your mind as you see that BP's have not been at goal?

Back 162

In ALLHAT, CKD as indicated by a serum creatinine of >1.5 mg/dL was a strong predictor of failure to achieve goal blood pressure.5 Treatment resistance in patients with CKD is undoubtedly related in large part to increased sodium and fluid retention and consequential intravascular volume expansion.

Front 163

What are the risk factors for renal artery stenosis?

Back 163

More than 90% of renal artery stenoses are atherosclerotic in origin.91 The likelihood of atherosclerotic renal artery stenosis is increased in older patients; in smokers; in patients with known atherosclerotic disease, especially peripheral arterial disease; and in patients with unexplained renal insuf- ficiency.

Front 164

What are the risk factors for bilateral renal artery stenosis?

Back 164

Bilateral renal artery stenoses should be suspected in patients with a history of "flash" or episodic pulmonary edema, especially when echocardiography indicates pre- served systolic heart function.

Front 165

What are the risk factors for fibromuscular dysplasia?

Back 165

Less than 10% of renal lesions are fibromuscular in etiology developing most commonly in women, <50 years of age.

Front 166

You suspect fibromuscular dysplasia in your young obese woman with BP's in >180/110, non-responsive to treatment. What is your diagnostic test of choice?

Back 166

Duplex ultrasound, magnetic resonance angiography (MRA), renal scintigraphy, and computed tomography (CT) angiography have good test characteristics in published studies, but the true positive and negative predictive value will vary both with the populations at risk and the level of expertise at each institution. Negative imaging studies warrant additional examinations for patients in whom there is a high level of clinical suspicion and for whom renal revascularization is being seriously considered.

Front 167

What are the complications of urinary retention?

Back 167

Complications include infection and renal failure.

Front 168

How does urinary retention from bladder CA usually present?

Back 168

Urinary retention from bladder tumors is usually caused by blood clots from intravesicular bleeding and often presents with painless hematuria.

Front 169

You insert a foley for a man with BPH. What treatment improves the likelihood of trial of void?

Back 169

In men with benign prostatic hyperplasia, initiation of treatment with alpha blockers at the time of catheter insertion improves the success rate of trial of voiding without catheter.

McNeill SA, Hargreave TB, for the Members of the Alfaur Study Group. Alfuzosin once daily facilitates return to voiding in patients in acute uri- nary retention. J Urol. 2004;171(6 pt 1):2316-2320.

Lucas MG, Stephenson TP, Nargund V. Tamsulosin in the management of patients in acute urinary retention from benign prostatic hyperplasia. BJU Int. 2005;95(3):354-357.

Front 170

What is the long term treatment of BPH that prevents acute urinary retention?

Back 170

Prevention of acute urinary retention in men with benign prostatic hyperplasia may be achieved by long- term treatment with 5-alpha reductase inhibitors.

Front 171

What kind of foley do you use for patients requiring long-term catheterization?

Back 171

Silver alloy-impregnated urethral catheters reduce the incidence of urinary tract infections in hospitalized patients requiring catheterization for up to 14 days.

Brosnahan J, Jull A, Tracy C. Types of urethral catheters for manage- ment of short-term voiding problems in hospitalised adults. Cochrane Database Syst Rev. 2004;(1):CD004013.

Front 172

What kind of foley do you recommend for neurogenic bladder?

Back 172

Low-friction, hydrophilic-coated catheters increased patient satisfaction and decreased urinary tract infection and hematuria in patients with neurogenic bladder who practice clean, intermittent self-catheterization.

De Ridder DJ, Everaert K, Fernandez LG, et al. Intermittent catheterisation with hydrophilic-coated catheters (SpeediCath) reduces the risk of clini- cal urinary tract infection in spinal cord injured patients: a prospective randomised parallel comparative trial. Eur Urol. 2005;48(6):991-995.

Vapnek JM, Maynard FM, Kim J. A prospective randomized trial of the LoFric hydrophilic coated catheter versus conventional plastic catheter for clean intermittent catheterization. J Urol. 2003;169(3):994-998.

Front 173

What are the signs and symptoms of BPH?

Back 173

Patients will gener- ally present with a history of multiple lower urinary tract voiding symptoms, including frequency, urgency, nocturia, straining to void, weak urinary stream, hesi- tancy, sensation of incomplete bladder emptying, and stopping and starting of urinary stream. Prior history of catheterizations.

Front 174

What percent of men with BPH will have recurrent retention after foley catheter dc?

Back 174

up to 70 percent of men will have recurrent urinary retention within one week if the bladder is simply drained.

Front 175

Your patient keeps failing trial of void. When do you consider surgery?

Back 175

American urological association (aua) guidelines recommend at least one attempted trial of voiding after catheter removal before considering surgical intervention.

Front 176

What percent of hematochezia is caused by UGIB?

Back 176

Although approximately 10% to 15% of patients presenting with acute severe hematochezia have an upper GI source of bleeding identified on up- per endoscopy, the most common causes of lower GI bleeding are divertic- ulosis, hemorrhoids, ischemic colitis, and angiodysplasia

Front 177

What are the clinical features of ischemic colitis?

Back 177

Lower GI bleeding preceded by hypovolemia suggests ischemic colitis

Front 178

In what percent of patients will diverticular bleeding recur?

Back 178

Bleeding recurs in 14% to 38% of cases following the primary episode and in up to 50% of cases following a second episode of bleeding

Front 179

What are the two types of radiation proctitis?

Back 179

There are 2 forms of radiation proctopa- thy, acute and chronic. The acute form occurs in nearly all patients.1 The incidence of the chronic form ranges from 2% to 20%.

Front 180

What is the definition of CHRONIC radiation proctitis?

Back 180

Symptoms that persist 3 months after the completion of radiation therapy or symptoms that begin 3 months after the initiation of radiation therapy.

Front 181

Should you biopsy patients with radiation proctitis?

Back 181

The presence of an inflamed mucosa should not be assumed to be due to radiation without confirmation of the cause by biopsy

Front 182

What is better for radiation proctitis - oral sulphaslazine or sucralfate?

Back 182

RCT of oral sulphasalazine (500 mg TID) plus rectal steroids (prednisolone 20 mg) against rectal sucralfate (2 g twice a day) for 8 weeks in 37 patients with CRP. 53% vs 94% improvement in symptoms respectively.
Kochhar R, et al. Dig Dis Sci 1991;36

Front 183

Does metronidazole confer any benefit to chronic radiation proctitis? What is the evidence for or against it?

Back 183

RCT - 60 patients given oral mesalazine (3 g per day) and betamethasone enema with or without oral metronidazole 400 mg three times a day for 1 year. Ninety-two per cent of the metronidazole group had a reduction in rectal bleeding compared with 42% in the other group.
Cavcic J, et al. Croat Med J 2000;41:314e318.

Front 184

When medical therapy and APC fail for chronic radiation proctitis, what is the next step?

Back 184

Hyperbaric oxygen seems to be effective when other therapies fail d eight of 10 patients who had failed medical therapy or laser therapy responded to hyperbaric oxygen
Jones K, et al. Radiother Oncol 2006;78: 91e94.

Front 185

Whats the mortality rate of sespsis when hypotension and lactate >4 occur?

Back 185

the mortality of septic patients presenting with both hypotension and lactate ≥ 4 mmol/L is 46.1%

Front 186

You cannot measure ScVO2 in a patient with sepsis. What is your lactate goal?

Back 186

A trial reported that early quantitative resuscitation based on lactate clearance (decrease by at least 10%) was noninferior to early quantitative resuscitation based on achieving ScvO2 of 70% or more.
Jones AE et al. EMShockNet JAMA 2010; 303: 739-746

Front 187

When is it better to use dopamine in septic shock than norepineprhine?

Back 187

We suggest dopamine as an alternative vasopressor agent to norepinephrine only in highly selected patients (eg, patients with low risk of tachyarrhythmias and absolute or relative bradycardia)

Front 188

When is it better to use phenylephrine than norepinephrine in septic shock?

Back 188

Phenylephrine is not recommended in the treatment of sep- tic shock except in the following circumstances: (a) norepi- nephrine is associated with serious arrhythmias, (b) cardiac output is known to be high and blood pressure persistently low, or (c) as salvage therapy when combined inotrope/ vasopressor drugs and low-dose vasopressin have failed to achieve the MAP target

Front 189

What is the physiology of phenylephrine?

Back 189

With its almost pure α-adrenergic effects, phenylephrine is the adrenergic agent least likely to produce tachycardia, but it may decrease stroke volume and is therefore not recommended for use in the treatment of septic shock except in circumstances where norepinephrine is: a) associated with serious arrhythmias, or b) cardiac output is known to be high, or c) as salvage therapy when other vasopressor agents have failed to achieve target MAP

Front 190

What were the results of the VASST trial?

Back 190

The VASST trial, an RCT comparing norepinephrine alone to norepinephrine plus vasopressin at 0.03 U/min, showed no difference in outcome in the intent-to- treat population

Front 191

What did the Annane study of JAMA 2002 show?

Back 191

This French multicenter RCT of patients in vasopressor-unrespon- sive septic shock (hypotension despite fluid resuscitation and vasopressors for more than 60 mins) showed significant shock reversal and reduction of mortality rate in patients with rela- tive adrenal insufficiency (defined as postadrenocorticotropic hormone [ACTH] cortisol increase ≤ 9 μg/dL)

Front 192

What did the CORTICUS trial show?

Back 192

In contrast, a large, European multicenter trial (CORTICUS) that enrolled patients without sustained shock and had a lower risk of death than the French trial failed to show a mortality benefit with steroid therapy (178). Unlike the French trial that only enrolled shock patients with blood pressure unresponsive to vasopressor therapy, the CORTICUS study included patients with septic shock regard- less of how the blood pressure responded to vasopressors; the study baseline (placebo) 28-day mortality rate was 61% and 31%, respectively. The use of the ACTH test (responders and nonresponders) did not predict the faster resolution of shock.

Front 193

Should you measure cortisol levels before giving hydrocortisone in septic shock?

Back 193

Random cortisol levels may be useful for absolute adrenal insufficiency; however, for septic shock patients who suffer from relative adrenal insufficiency (no adequate stress response), random cortisol levels have not been demonstrated to be useful. No evidence of this distinction was observed between responders and nonresponders in a recent multicenter trial

Front 194

What is your threshold for using Bicarb in sepsis?

Back 194

We recommend against the use of sodium bicarbonate therapy for the purpose of improving hemodynamics or reducing vasopressor requirements in patients with hypoperfusion-induced lactic acidemia with pH ≥ 7.15

Front 195

What was the outcome of the Kumar study Crit Care Medicine 2006?

Back 195

Objective: To determine the prevalence and impact on mortal- ity of delays in initiation of effective antimicrobial therapy from initial onset of recurrent/persistent hypotension of septic shock.
Design: A retrospective cohort study performed between July 1989 and June 2004.
Setting: Fourteen intensive care units (four medical, four sur- gical, six mixed medical/surgical) and ten hospitals (four aca- demic, six community) in Canada and the United States.
Patients: Medical records of 2,731 adult patients with septic shock.
Interventions: None.
Measurements and Main Results: The main outcome measure was survival to hospital discharge. Among the 2,154 septic shock patients (78.9% total) who received effective antimicrobial ther- apy only after the onset of recurrent or persistent hypotension, a strong relationship between the delay in effective antimicrobial initiation and in-hospital mortality was noted (adjusted odds ratio 1.119 [per hour delay], 95% confidence interval 1.103-1.136, p < .0001). Administration of an antimicrobial effective for isolated or suspected pathogens within the first hour of documented hypo-
tension was associated with a survival rate of 79.9%. Each hour of delay in antimicrobial administration over the ensuing 6 hrs was associated with an average decrease in survival of 7.6%. By the second hour after onset of persistent/recurrent hypotension, in-hospital mortality rate was significantly increased relative to receiving therapy within the first hour (odds ratio 1.67; 95% confidence interval, 1.12-2.48). In multivariate analysis (including Acute Physiology and Chronic Health Evaluation II score and therapeutic variables), time to initiation of effective antimicrobial therapy was the single strongest predictor of outcome. Median time to effective antimicrobial therapy was 6 hrs (25-75th per- centile, 2.0 -15.0 hrs).
Conclusions: Effective antimicrobial administration within the first hour of documented hypotension was associated with in- creased survival to hospital discharge in adult patients with septic shock. Despite a progressive increase in mortality rate with increasing delays, only 50% of septic shock patients received effective antimicrobial therapy within 6 hrs of documented hypo- tension. (Crit Care Med 2006; 34:1589-1596)

Front 196

Risk factors for fungemia?

Back 196

organ transplantation, chemotherapeutic agents, invasive monitoring devices, parenteral nutrition, broad-spectrum antimicrobial agents, and assisted ventilation

Front 197

In patients with fungemia what the worst prognostic signs?

Back 197

High APACHE II scores, inadequate initial therapy, lack of antifungal therapy, and failure to remove central venous catheters were consistently identified as independent risk factors influencing mortality in fungemic patients

Front 198

What did the SAFE study in the use of albumin as a resuscitative fluid show?

Back 198

In patients in the ICU, use of either 4 percent albumin or normal saline for fluid resus- citation results in similar outcomes at 28 days.
SAFE study group. N engl j med 2004: 350;22

Front 199

Your patient with septic shock is not responding to dopamine or dobutamine, and you decide on epinephrine. What do you see in terms of your hemodynamic parameters?

Back 199

In patients with baseline RV failure, epinephrine infusion significantly increased MAP, and CI without any change in SVR, heart rate, or PAOP. In patients without RV failure (group B), RV para- meters remained unchanged during epinephrine admin- istration.

Front 200

What are the two main causes of ventilator associated lung injury?

Back 200

Ventilator- induced lung injury may be caused by overdistention of aerated lung regions, especially when large tidal volumes are used. Ventilator-induced lung injury may also occur if a substantial portion of the lung is not aerated at end-expiration because of atelectasis, flooding, and consolidation.

Front 201

What are your respiratory variables desires in patients mechanically ventilated with ARDS?

Back 201

A tidal-volume goal of 6 ml per kilogram of predicted body weight and an inspiratory plateau pressure of 30 cm of water or less. Aim for PEEP between 5 and 12 cmH20, no greater.

Front 202

What are the features of serum sickness?

Back 202

The cardinal features of serum sickness are rash, fever, and polyarthralgias or polyarthritis, which begin one to two weeks after first exposure to the responsible agent, and resolve within a few weeks of discontinuation.

Front 203

What is the pathophysiology of serum sickness?

Back 203

Type 3 HS - This syndrome was revealed to result from the generation of human antibodies to horse serum proteins, subsequent deposition of antigen-antibody (immune) complexes in tissues, and activation of the complement cascade. Complement activation and recruitment of leukocytes lead to the release of inflammatory mediators, including histamine, the mediator likely responsible for the urticarial lesions classically observed.

Front 204

What is the earliest manifestation of serum sickness and what clinical features are specific to its presentation?

Back 204

Almost all patients diagnosed with serum sickness develop a pruritic rash, which is often the earliest clinical feature. The mucous membranes are not involved, which can be a useful feature in distinguishing serum sickness from clinically similar conditions.

Front 205

How do you diagnose and treat Q fever endocarditis?

Back 205

Dukes criteria is still used and was modified to include Coxiella burnettii. A diagnosis requires a phase 1 titer of IgG > 800 or a phase II titer of IgG >200 and IgM >50. The organism is difficult to eradicate and requires a minimum duration of 18 months of treatment with doxycycline and hydroxychloroquine.

Front 206

What is Loffler's endocarditis?

Back 206

Hypereosinophilia (either idiopathic or from a parasitic infection) can damage the heart in 2 ways - endomyocardial fibrosis (Davies disease) and eosinophilic endocarditis (Lofflers endocarditis). If was first reported in 1968 by Hard and Anderson. Commonly the heart wall will develop large mural thrombi (thrombi which lay against the ventricle walls) due to the deterioration of LV wall muscle from presumed direct eosinophilic damage. Symptoms include edema and breathlessness. The disease is commonly contracted in temperate climates (due to the favorable conditions for parasites), and is rapidly fatal.

Front 207

Is there any role for monitoring Epstein-Barr virus reactivation in a patient post-renal transplant on immunosuppression?

Back 207

Post-transplant lymphoproliferative disorder (PTLD) is among the more common malignancies seen after solid organ transplantation. Most cases are related to EBV. In the setting of immunosuppression, a reservoir of previously EBV-infected B-cells is permitted to clonally expand. Many centers now screen for EBV reactivation to identify early PTLD in post-transplant patients. Early detection of rising EBV levels allows for tapering of immunosuppression and other interventions, including rituximab.

Front 208

What vaccinations are mandatory for patients going to Mecca for Hajj?

Back 208

For patients going to Mecca, it is mandatory that they obtain a vaccination against meningitis. Experts in the Middle East region recommend the use of conjugate vaccines instead of plain polysaccharide vaccines given the potential of the polysaccharide to stop transmission of carriers. Menactra brand vaccine is conjugated to diphtheria and Menveo brand is conjugated to mutant diphtheria toxin.

Front 209

Whats better for advanced CHF, pulsatile or continuous flow LVAD?

Back 209

Treatment with a continuous-flow left ventricular assist device in patients with ad- vanced heart failure significantly improved the probability of survival free from stroke and device failure at 2 years as compared with a pulsatile device.

Front 210

What is the effect of morphine on venous capacitance? Does fentanyl have the same effect? How can it be reversed?

Back 210

Morphine has a histamine-induced venodilatory effect. Fentanyl does not have this effect at all. The effect can be reversed by Diphenhydramine or Famotidine, but not by naloxone.

Front 211

What are the histopathological characteristics of the anti-phospholipid syndrome?

Back 211

Arterial (usually cerebral circulation) and venous thrombosis (deep veins of legs) should be present without evidence of inflammation in the vessel wall.

Front 212

What are the obstetrical characteristics of anti-phospholipid syndrome?

Back 212

They include the unexplained death of one or more morphologically normal fetuses at or beyond the 10th week of gestation, the premature birth of one or more morphologically normal neonates before the 34th week of gestation because of either eclampsia or severe preeclampsia, and three or more unex- plained, consecutive spontaneous abortions before the 10th week of gestation.

Front 213

What is the cause of an acutely elevated creatinine in DKA?

Back 213

Dehydration may develop during DKA from osmotic diuresis resulting in prerenal acute kidney injury. Acetoacetate has also been found to interfere with alkaline picrate assay (but not high-performance liquid chromatography), resulting in a falsely elevated creatinine.
Kemperman et al. Journal of Internal Medicine 2000;248:511-517

Front 214

What is the role of pancreatic enzyme supplementation in treating the pain of chronic pancreatitis?

Back 214

Trials report mixed data, but the use of non-enteric coated enzymes has shown efficacy in some studies. This formulation must be administered with PPIs or H2 blockers to prevent digestion of the medication in the stomach. Non-enteric preparations are actually not approved for use in the US. Newer enteric coated preparations are available, but do not have robust trial data to support them.

Isaksson et al. Dig Dis Sci 1983;28(2):97-102

Front 215

What are the cardiac manifestations of Friedreich's Ataxia?

Back 215

Friedreich's Ataxia (FA) is an autosomal recessive spinocerebellar ataxia. FA is associated with a progressive hypertrophic cardiomyopathy that is a common cause of death due to arrhythmias or cardiac failure. Patients usually present with a cardiomyopathy less than 40 years old. The typical pattern is concentric left ventricle hypertrophy. Global systolic function is usually preserved early on and only end-stage patients with cardiomyopathy develop a reduced ejection fraction with global hypokinesia and a slightly dilated left ventricle.

Weidemann et al. Journal of Neurochemistry 2013;126:88-93

Front 216

What are the roles of D-dimer and ultrasound in risk stratifying patients with VTE?

Back 216

Based on weak evidence, the 2012 ACCP guidelines recommend in first unprovoked proximal DVT or PE to continue lifelong anticoagulation in those with low and intermediate risk of bleeding. Debate still remains, however, regarding the duration of anticoagulation in this patient population. D-dimer has been shown prospectively to help in risk stratifying patients after three months of anticoagulation, while repeat ultrasound has had mixed evidence in supporting its use in risk stratification. The ongoing DULCIS trial will assess the utility of a combined D-dimer and ultrasound at three months to help further risk stratify recurrence.

Carrier et al. J Thromb Haemost 2011;9(6):1119-25

Front 217

What kind of pacemaker would you choose for sick sinus syndrome?

Back 217

Assume the patient has sinus node dysfunction accompanying disease of the atrioventricular node or His bundle, bundle-branch block, or a requirement for therapy with drugs that slow atrioventricular-node conduction, such as beta-blockers or calcium-channel blockers, a dual-chamber (DDD) system is appropriate, regardless of the patient's age.

Front 218

What kind of pacemaker would you choose for a patient with sick sinus and intermittent atrial tachyarrhythmias?

Back 218

If a patient with sinus-node dysfunction has intermit- tent atrial tachyarrhythmias, a pacemaker that can be programmed to the DDI or DDIR mode or that has specialized algorithms to detect tachycardia should be considered.

Front 219

How can you tell on an ECG that a patient has a Bi Ventricular pacer?

Back 219

Pacing comes from the LV. QRS complex is down in I and up in V1 (depol from L to R). This kind of pacer is considered DDD in the LV.

Front 220

What kind of pacer would you choose for a patient with Atrial fibrillation with a slow ventricular response (AV node dz)?

Back 220

Choose VVI (pace the ventricle, sense from the ventricles, and only inhibit the signal if you get a native beat). You don't want to atrial sense since the atria are going at ~400 bpm.

Front 221

What is Ashman phenomenon in Atrial Fibrillation?

Back 221

The refractory period of the Purkinje cells of the bundle branches and fascicles is importantly determined by the preceding cycle length: A long preceding cycle lengthens and a short preceding cycle shortens the refractory period in these structures. A long-short cycle, then, predisposes to aberration. The initiation of aberration occurs with a long-short or more likely a short-long-short interval that leads to conduction block in one of the bundle branches, usually the right bundle, due to alterations of variations and refractoriness between the two bundles. Aberration can be in both bundles so that there is alternating bundle branch block and there can also be something called "concealed perpetuated aberration."

Front 222

How low of a temperature do you have to target for therapeutic hypothermia?

Back 222

Systemic cooling to a bladder temperature between 32°C and 34°C for 24 hours increased the chance of survival and of a favorable neurologic outcome (a cerebral- performance category of 1 or 2), as compared with standard normothermic life support.

Holzer et. al. 2002 N Engl J Med, Vol. 346, No. 8

Front 223

What are the clinical features of severe asthma exacerbation?

Back 223

Accessory muscle activity, paradoxical pulse exceeding 25 mmHg, heart rate greater than 100 beats/minute, respiratory rate greater than 25-30 breaths/minute, limited ability to speak, peak expiratory flow rate or forced expiratory volume in 1 s less than 50% of predicted, and an arterial oxygen saturation less than 91-92%

Front 224

What happens to FRC in acute severe asthma?

Back 224

Acute severe asthma is characterized by pulmonary hyperinflation, with an increase in functional residual capacity of up to twice the normal values in very severe cases. The mechanism of this hyperinflation consists in the critical limitation of the expiratory flow - 1) low elastic recoil and 2) high outward recoil of the chest wall generated by the persistent activation of the inspiratory muscles during expiration

Front 225

What is the goal of vent management in patients with severe acute asthma?

Back 225

The primary focus must be on avoiding excessive airway pressure and minimizing lung hyperinflation. To achieve this goal it is often necessary to hypoventilate the patient and thus to tolerate hypercapnia.

Front 226

What are the two most common complications of mechanical ventilation in severe asthma?

Back 226

The most frequently reported complication of me- chanical ventilation in patients with acute severe asthma is hemodynamic instability manifested as hypotension, usually occurring at the initiation of ventilation and related to the decrease in systemic venous return caused by worsening of hyperinflation.

Barotrauma is the second most frequently reported complication. Controlled hypoventilation does not confer complete protection in this context

Front 227

What are the absolute contraindications for non-invasive ventilation?

Back 227

Absolute contraindications for the use of NIPPV in asthma are the same as in other conditions [80], including emergency intubation for cardiorespiratory resuscitation, hemodynamic and electrocardiographic instability, life-threatening hypox- emia, and an altered state of consciousness.

Front 228

What are the initial goal settings of patients with acute asthma who go onto biPAP?

Back 228

NIPPV can be started with low levels of inspi- ratory pressure support (5-7 cmH2 O) and PEEP (3-5cmH20, see previous discussion). Pressure sup- port should be progressively increased (by 2cmH2O every 15 min), the goal being to reduce respiratory rate below 25 breaths/minute, while keeping peak inspiratory pressure below 25 cmH2O.

Front 229

What are the goal ventilatory settings for patients with acute asthma who undergo intubation?

Back 229

The way to minimize hyperinflation essentially consists in keeping minute ventilation down (i.e., ≤ 10 l/min in the average adult patient) and expiratory time up (≥ 4 s). Once a ventilatory pattern consistent with these goals has been achieved, there is probably little to be gained by further fiddling with machine settings.

Front 230

First sign of an evolving inferior wall MI?

Back 230

Flipped T wave in aVL

Front 231

Is there a difference between the clinical characteristics of overt and occult OBSCURE GIB?

Back 231

There were no significant differences in the prevalence rates of comorbidities or rates of use of medications between the patients with overt and occult OGIB.

Sakai E, Endo H Digestive Endoscopy 2012

Front 232

What did the PRAMI study show?

Back 232

In patients with STEMI and multivessel coronary artery disease undergoing infarct-artery PCI, preventive PCI in noninfarct coronary arteries with major stenoses significantly reduced the risk of adverse cardiovascular events, as compared with PCI limited to the infarct artery.

Wald D, et. al. NEJM 2013 369; 12 pp 1115

Front 233

What is stress urinary incontinence?

Back 233

Involuntary loss of urine on physical exertion, sneezing, or couging.

Front 234

What's the first step in the management of stress urinary incontinence?

Back 234

Initial midurethral slin surgery, as compared with initial physiotherapy, results in higher rates of subjective improvement and subjective and objective cure at 1 year.

Labrie J, et al NEJM 2013 369; 12 pp 1124

Front 235

What percent of strokes are caused by carotid artery disease?

Back 235

Carotid artery disease causes approximately 10 to 20% of strokes.

Front 236

Your patient has repeated TIAs that are brief (<1 minute), with some limb shaking. What is the etiology of these episodes?

Back 236

This is likely due to reduced flow due to high-grade stenosis causing symptoms referable to brain regions at the border zones between the anterior, middle, and posterior cerebral arteries, where perfusion pressure is the lowest and most often vulnerable to further reduction. Embolic TIAs tend to be longer (5 to 30 minutes).

Front 237

What diameter of carotid artery is associated with the highest risk of stroke?

Back 237

A 2-mm residual luminal diameter or a 60-70% reduction in diameter associated with a marked increase in the risk of stroke.

Front 238

Your young patient in a motor vehicle accident experiences unilateral neck, facial, and head pain. They also experience random episodes of monocular blindness. What is your diagnosis?

Back 238

Dissection of the carotid artery. >60% experience neck, head, and facial pain. Often associated with TIA or stroke. Horners syndromes may be present.

Front 239

Your young patient with stroke experiences Horners syndrome and is worked up and found to have carotid dissection. What is your diagnosis?

Back 239

Suspect collagen abnormalities such as Type 4 Ehlers Danlos Syndrome.

Front 240

A 50 year old has intracranial aneurysms and carotid dissection. What is your diagnosis?

Back 240

Fibromuscular dysplasia. Fibrotic thickening of the arterial wall, most often the media. Prescribe aspirin for stroke prevention.

Front 241

Your patient is diagnosed with carotid artery stenosis. What is the first step?

Back 241

Control smoking, high blood pressure, and hyperlipidemia.

Front 242

What did the NASCET trial show?

Back 242

Among patients with stenosis of 70% or more, the 2-year risk of ipsilateral stroke was 9% in the carotid endarterectomy (plus medical therapy) vs 26% in the group assigned to medical therapy alone.
A meta-analysis showed that endarterectomy has the biggest impact when done within 2 weeks after stroke.

Front 243

You pick up a carotid artery stenosis of 60% in a patient that is completely asymptomatic. What do you do?

Back 243

Lifestyle modification, statin, and anti-HTN. The benefits of of carotid endarterectomy or carotid stenting in addition to medical therapy, as compared with current medical therapy alone, are uncertain in patients with asymptomatic carotid stenosis, especially women.

Front 244

In HIV-associated Kaposi's sarcoma, what is the mainstay of treatment?

Back 244

ART and chemotherapy. The overall rate of survival in Kaposi's is the same in ART with and without chemo but combination has a higher response rate and progression-free survival than does ART alone.

Front 245

In Kaposi's sarcoma, does treatment of HHV8 have any role?

Back 245

Ganciclovir seems to protect patients with AIDS from the development of Kaposi's, but there is no apparent role for such treatment once Kaposi's occurs, perhaps because the HHV8 is mainly in a latent form by the time the tumor is established.

Front 246

You patient is on metformin + pioglitazone for T2DM and they are now requiring a third agent. What would you go for?

Back 246

Sitagliptin should be preferred to glibenclamide as an addition to the metformin + pioglitazone combination for its better protection of beta-cell secretion and its neutral effect on body weight.
Derosa G, Cicero AF, Franzetti IG, et al. Diabet Med. 2013 Jul;30(7):846-54.

Front 247

How does Sitagliptin (Januvia) work?

Back 247

Sitagliptin works to competitively inhibit the enzyme dipeptidyl peptidase 4 (DPP-4). This enzyme breaks down the incretins GLP-1 and GIP, gastrointestinal hormones released in response to a meal.[13] By preventing GLP-1 and GIP inactivation, they are able to increase the secretion of insulin and suppress the release of glucagon by the pancreas.

Front 248

Is there any benefit to daily interruptions of sedation in mechanically ventilated patients? What are the long-term outcomes of patients that have interruptions of sedation?

Back 248

There are proven benefits of sedation interruptions, including a mortality benefit at one year.
A wake up and breathe protocol resulted in similar cognitive, psychological, and functional outcomes at 3 and 12 months post-ICU.

Front 249

Your mechanically ventilated patient develops a pneumonia. How long do you treat for?

Back 249

Among patients who had received appropriate initial empirical therapy, with the possible exception of those developing nonfermenting gram-negative bacillus (Pseudomonas) infections, comparable clinical effectiveness against VAP was obtained with the 8- and 15-day treatment regimens. The 8-day group had less antibiotic use.

Chastre JAMA. 2003;290:2588-2598

Front 250

How can you RULE IN a pneumonia using CRP to distinguish it from CHF?

Back 250

CRP increases of ≥0.56 mg/L/h were diagnostic of pneumonia. CRP levels on admission (~127) together with CRP increases had a sensitivity of 0.96 and a specificity of 0.972 (p b 0.001) as markers to distinguish pneumonia from ADHF.

Joffe et al. Clinical Biochemistry 42 (2009) 1628 - 1634

Front 251

What is the annual incidence of VTE?

Back 251

the annual incidence of VTE has been relatively constant, at about 1 event per 1000 person-years since 1979.

Front 252

What are the biggest risk factors for VTE?

Back 252

3 categories: 10 items
1) endothelial damage
surgery, trauma, previous central vein catheterization, or transvenous pacemaker placement
2) hypercoagulability
malignant neoplasm with and without concurrent chemotherapy, previous superficial vein thrombosis, varicose veins (especially in young people)
3) Stasis
hospital or nursing home inpatient status, neurologic disease with extremity paresis, and congestive heart failure

Heit J et al Arch Intern Med. 2000;160(6):809-815

Front 253

Are BMI and smoking risk factors for VTE?

Back 253

Neither BMI nor current or past tobacco smoking was an independent risk factor for VTE.

Heit J et al Arch Intern Med. 2000;160(6):809-815

Front 254

Are pregnancy or tamoxifen associated with increased VTE?

Back 254

Among women, pregnancy, postpartum period, oral contraceptive use, hormone therapy, and tamoxifen therapy were not independent risk factors for VTE.

Heit J et al Arch Intern Med. 2000;160(6):809-815

Front 255

Your inpatient has a negative duplex. What is the risk they will develop DVT in the next 3 months after hospitalization?

Back 255

Although withholding anticoagulant therapy after a single negative whole-leg ultrasonography seems to be safe, up to 3.5% of inpatients may nevertheless develop venous thromboembolism in the next 3 months.

Sevestre, M et al Am J Med, 2010 Vol 123

Front 256

What is the standard of care for Acute Promyelocytic Leukemia?

Back 256

ATRA + Arsenic Trioxide or ATRA + Anthracycline based chemo (e.g. idarubicin). Most common side effects of ATRA-Arsenic Trioxide include Hepatotoxicity and prolongation of the QTc. Hematologic side effects include Neutropenia and Thrombocytopenia.

Lo-Coco NEJM 2013, 369. 111

Front 257

What is the mechanism of action of Ipilimumab in melanoma? Nivolumab?

Back 257

Ipilimumab targets the Cytotoxic T lymphocyte associated antigen 4 (CTLA4). Nivolumab targets the programmed death 1 receptor (PD-1).

Front 258

An 18 year old adopted white woman presents to your office at the age of 15 with absent breast development, primary amenorrhea, and intermitent lower abdominal pain. The patient was underweight (BMI 16), had Tanner stage 1 breast development, and Tanner stage 4 pubic hair. She had severe facial acne. Estradiol was very elevated, LH nml, FSH nml, 46XX karyotype. Ultrasound revealed small uterus and enlarged multicystic ovaries. What is your diagnosis? Explain the gonadotropin levels.

Back 258

This patient can make gonadotropins and estrogens. The manifestations of her disease were inability to respond to the estrogen (estrogen resistance, e.g. small breasts, small uterus). Instead of very high LH, FSH levels expected, this patient had normal levels of gonadotropins. The reason is that she had Inhibin A levels that were markedly elevated (which suppresses FSH). Given her facial acne, one could assume her testosterone was high enough to suppress LH. The patient was found to have biallelic mutations to estrogen receptor 1 (ESR1 mutation).

Front 259

Your patient in the CCU undergoes PCI and subsequently needs insulin for hyperglycemia. How aggressively do you manage his glucose?

Back 259

Intensive use of insulin to regulate hyperglycemia in acute coronary syndrome (ACS) patients did not reduce infarct size, and may have caused harm. This was found in all patients, not just diabetics.
de Mulder M et al JAMA Intern Med. September 09, 2013

Front 260

Your patient with prior MI is taking a sulfonylurea for diabetes. What do you do?

Back 260

Stop it. Increased risk of CV disease and all cause mortality is associated with sulfonylurea use. Sulfonylureas include:
First generation
Carbutamide, Acetohexamide, Chlorpropamide, Tolbutamide, Tolazamide
Second generation
Glipizide, Gliclazide, Glibenclamide (glyburide), Glibornuride, Gliquidone, Glisoxepide, Glyclopyramide, Glimepiride

Front 261

Whats the mechanism of action of sulfonylureas?

Back 261

Sulfonylureas bind to an ATP-dependent K+(KATP) channel on the cell membrane of pancreatic beta cells. This inhibits a tonic, hyperpolarizing efflux of potassium, thus causing the electric potential over the membrane to become more positive. This depolarization opens voltage-gated Ca2+ channels. The rise in intracellular calcium leads to increased fusion of insulin granulae with the cell membrane, and therefore increased secretion of (pro)insulin.

Front 262

Your patient with a Hgb A1C 7% after one year of diagnosis of diabetes. What do you do?

Back 262

You must intensify therapy. In 110,000 patients with hemoglobin A1c of 7% or higher a year after diabetes diagnosis, those who didn't intensify treatment (addition of a second oral drug or insulin) within a year were significantly more likely to have a myocardial infarction, stroke or heart failure during study follow-up, supporting the cardiovascular benefits of early treatment intensification in patients with poor glycemic control, researchers concluded.

Front 263

Your patient suffers an acute ankle sprain. What topical therapies are available? Do you suggest PT or home exercise program?

Back 263

Topical Traumeel (a natural treatment) and Diclofenac decreased pain and improved joint function to the same extent in acute ankle sprain.
de Vega CG Int J Clin Pract. 2013 Jul 25

Manual therapy is superior to home exercise.
Cleland JA, J Orthop Sports Phys Ther. 2013;43(7):443-55.

Front 264

Is the dipeptidyl peptidase-4 inhibitor alogliptin for T2DM associated with adverse outcomes? How about rosiglitazone?

Back 264

Analyses have not shown a signal of increased CV risk with alogliptin or rosiglitazone in patients with type 2 diabetes.
White WB, et al. Diabetes Obes Metab. 2013 Jul;15(7):668-73.
Bach RG, et al. Circulation. 2013 Aug 20;128(8):785-794.

Front 265

Your eldely patient is admitted and you wonder whether she is going to develop a pressure ulcer. What do you do?

Back 265

Mini Nutritional Assessment was able to predict the development of PUs. A MNA score of less than 8 performed better than the SGA, Braden Scale, and plasma arginine levels in predicting PU development. Although lower plasma arginine concentration at time of admission was associated with PU development, the AUC for arginine was not significantly different from 0.50. The findings from this prospective study support the use of nutritional assessment in inpatients to predict PU risk and target appropriate interventions.

Yatabe MS, et al. J Am Geriatr Soc. 2013 Sep 19.

Front 266

Your overweight patient with knee osteoarthritis needs to lose weight and you recommend diet but will exercise make things worse?

Back 266

A 10% reduction in body weight is your goal. Diet + exercise is superior.
Messier SP, et al. JAMA. 2013 Sep 25;310(12):1263-73.

Front 267

What is the significance of relative bradycardia to predict the etiology of the infectious disease?

Back 267

Relative bradycardia as a clinical sign is when the pulse is less than expected at a given body temperature or a pulse-temperature dissociation. This physical finding has historically been associated with specific infectious agents, including intracellular organisms such as salmonella, legionella and chlamydia. However the presence of relative bradycardia is a poor predictor of specific infections. One study found that relative bradycardia, as a clinical sign in an individual patient, held no predictive value regarding the likely type of infection. Relative bradycardia as a characteristic feature of specific disease was found for typhoid fever, legionnaire's and chlamydia pneumonia.
Ostergaard et al. Journal of Infection 1996;33:185-191

Front 268

What is the prognosis of HIV-associated lymphoma as compared to non-HIV-associated lymphoma?

Back 268

About 70-90% of AIDS-related lymphomas are highly aggressive (usually DLBCL and Burkitt's). The relative risk of aggressive lymphoma in AIDS patients as compared with the generally population is 400-fold. In a study of patients in South Africa, it was found that despite HAART, the overall survival with DLBCL and HIV infection was significantly poorer than HIV negative patients with DLBCL (P<0.001). Additionally, HIV positive patients were significantly younger at presentation with greater likelihood of extranodal lymphoma.

Pather et al. Pathol Oncol Re 2013;19(4):695-705

Front 269

Which viruses cause Bell's palsy?

Back 269

Herpes simplex virus (HSV) activation has become widely accepted as the likely cause of Bell's palsy. In one study, HSV-1 genomes were identified in facial nerve endoneurial fluid and auricular muscle in 11 of 14 patients undergoing decompression surgery for Bell's palsy, but not in 12 controls. Herpes zoster is probably the second most common viral infection associated with facial palsy. Other infectious causes of Bell's palsy include cytomegalovirus, Epstein Barr virus, adenovirus, rubella virus, mumps, influenza B, and coxsackievirus. True prevalence of each infectious etiology is not known.

Murakami et al. Ann Intern Med 1996;124(1 Pt 1):27-30

Front 270

What is the pathophysiology of exercise-induced anaphylaxis?

Back 270

There are a spectrum of disorders including exercise-induced anaphylaxis and urticaria. These disorders usually start with sensitization by a food allergen up to several hours in advance of exercising. Common sensitizing foods include wheat, cereal, and shellfish. Although incompletely understood, proposed models to explain the pathophysiology include increased intestinal permeability, blood flow redistribution, and activation of tissue enzymes.

Barg et al. Curr Allergy Asthma Rep 2011;11(1):45-51

Front 271

Can excess muscle mass and creatine supplementation falsely reduce the estimated glomerular filtration rate (GFR)?

Back 271

GFR is often estimated with the MDRD equation which incorporates serum creatinine as a major variable. As creatinine is produced by muscle tissue, increased muscle mass can falsely elevate the creatinine. Creatine is an amino acid that undergoes non-enzymatic dehydration to form creatinine and can also cause false elevations in this value. Direct measurement of the 24-hour urine creatinine clearance can be used to obtain true measures of the GFR in these situations.

Refaie et al. Clin Nephrol 2007;68(4): 235-7

Front 272

What is the optimal hemoglobin target in patients with polycythemia vera?

Back 272

In a prospective randomized trial in 365 adults with JAK2-positive PV who were being treated with phlebotomy, hydroxyurea, or both, subjects were randomly assigned to either more intensive treatment (target hematocrit <45 percent) or less intensive treatment (target hematocrit 45 to 50 percent). After a median follow-up of 31 months, time until death from cardiovascular causes or major thrombotic events, was recorded in 5 of 182 patients in the lower hematocrit group (2.7 percent) and 18 of 183 patients in the higher hematocrit group (9.8 percent). The hazard ratio for the higher hematocrit group was 3.91 (95% CI 1.45-10.5). The rates of adverse events (ie, progression to myelofibrosis or myelodysplasia, leukemic transformation, bleeding) were not significantly different between the two treatment groups.

Marchioli et al. NEJM 2013;368(1):22

Front 273

How do you treat moderate to severe Crohn's disease?

Back 273

The SONIC trial has changed the management algorithm for moderate to severe Crohn's disease. The study was a randomized, double-blind trial, comparing infliximab or azathioprine alone versus combination therapy. 56% of patients on combination therapy compared to 44% on infliximab alone (P=0.02) and 30% on azathioprine alone (P<0.001) were in corticosteroid-free remission.

Colombel et al. NEJM 2010;362(15):1383-95

Front 274

What is Auto-Brewery Syndrome?

Back 274

Auto-Brewery Syndrome is gut overgrowth of yeast resulting in fermentation of carbohydrates into ethanol and persistent inebriation despite the lack of exogenous ethanol intake. Causative organisms have included Candida species and Saccharomyces cerevisiae. Treatment with antifungal therapy and carbohydrate restriction has been successful in case reports.

Cordell et al. International Journal of Clinical Medicine 2013;4(7):309-312

Front 275

What is acquired hemophilia A and how is it treated?

Back 275

Acquired hemophilia A, caused by an inhibitor of factor VIII, is an uncommon bleeding disorder that may be associated with underlying autoimmune disorders, malignancies, infections and medications, but is idiopathic in half of cases. Although steroids and cyclophosphamide are considered first-line agents, rituximab is emerging as second-line based on data from small case series.
Franchini et al. Blood 2008;112:250-255

Front 276

When is CRP useful for risk stratifying patients for goals of lipid-lowering therapy?

Back 276

The JUPITER trial found that patients with low-normal LDL and high CRP had reduction of both CRP and LDL, as well as lower rates of major cardiovascular events on statin compared to placebo. The Number Needed to Treat to prevent one event was 31 over 4 years.

Ridker et al. NEJM 2008;359:2195-2207

Front 277

What does the regimen of fixed schedule chlordiazepoxide for alcohol withdrawal consist of?

Back 277

Chlordiazepoxide every 6 hours for 12 doses (50mg x 4 followed by 25mg x8). In addition, their received 25-100mg of Chlordiazepoxide hourly when they achieved a CIWA score of 8 or greater ("as needed).

Saitz R., et. al JAMA 1994 (272) pp519

Front 278

What does the symptom triggered therapy protocol consist of?

Back 278

This group receives 25-100mg of chlordiazepoxide hourly when the CIWA score was 8 or greater.

Saitz R., et. al JAMA 1994 (272) pp519

Front 279

What treatment protocol, symptom triggered vs fixed dose, results in shorter medication treatment duration?

Back 279

Symptom triggered therapy.

Saitz R., et. al JAMA 1994 (272) pp519

Front 280

Does the severity of withdrawal symptoms (measured by CIWA) or incidence of delerium tremens differ between fixed dose or symptom triggered therapy?

Back 280

No. The greatest severity of withdrawal, incidence of delirium tremens, hallucinations, seizures, lethargy, AMA, and readmission did not differ between treatment groups.

Saitz R., et. al JAMA 1994 (272) pp519

Front 281

What is the clinical definition of delirium tremens?

Back 281

Cerebral manifestations: hallucinations, disorientation, agitation

Cardiac manifestations: tachycardia, hypertension

Sympathetic manifestations: fever, and diaphoresis

MUST be 48-96 hours after last drink.

Front 282

Your patient in the ER stopped drinking a few hours ago and came in. He suddenly gets very agitated and diaphoretic and confused. Is this DT?

Back 282

DT and alcoholic hallucinosis are NOT synonymous and symptoms that occur a few hours after the cessation of drinking, even if severe, are not manifestations of DT

Front 283

What are the risk factors for DTs?

Back 283

A history of sustained drinking
A history of previous DT
Age greater than 30
The presence of a concurrent illness
The presence of significant alcohol withdrawal in the presence of an elevated alcohol level
A longer period since the last drink (ie, patients who present with alcohol withdrawal more than two days after their last drink are more likely to experience DT than those who present within two days)

Front 284

What is the clinical benefit of interruption of sedation for patients mechanically ventilated in the ICU?

Back 284

In patients who are receiving mechanical
ventilation, daily interruption of sedative drug infusions decreases the duration of mechanical ventilation and the length of stay in the intensive care unit.

Kress J et al NEJM 2000 Vol 342, pp 1471

Front 285

Your patient has right sided chest pain. Does that decrease the likelihood of MI?

Back 285

Chest pain radiation to the right shoulder had a likelihood ratio of 2.9.

Panju. A., et. al. JAMA. 1998;280(14):1256-1263

Front 286

What features of the history of chest pain increase the likelihood the most?

Back 286

Pain in chest or left arm LR = 2.7
Chest pain radiation to Right shoulder LR=2.9
Chest pain radiation to Left arm LR=2.3
Chest pain radiation to Both left and right arm LR=7.1
Chest pain most important symptom LR=2.0
History of myocardial infarction LR = 2.0
Panju. A., et. al. JAMA. 1998;280(14):1256-1263

Front 287

What features of the ROS make MI most likely?

Back 287

Nausea or vomiting LR=1.9
Diaphoresis LR=2.0
Panju. A., et. al. JAMA. 1998;280(14):1256-1263

Front 288

What features of physical exam make MI most likely?

Back 288

S3 LR=3.2
SBP<80 LR=3.
Pulmonary crackles on auscultation LR=2.1
Panju. A., et. al. JAMA. 1998;280(14):1256-1263

Front 289

What features of history make MI LESS likely?

Back 289

PLEURITIC chest pain LR=0.2
SHARP or stabbing LR=0.3
POSITIONAL chest pain LR=0.3
reproduced by PALPATION LR=0.2-0.4*

Panju. A., et. al. JAMA. 1998;280(14):1256-1263

Front 290

What is the chance of an MI happening in the presence of a new Q wave?

Back 290

New Q wave LR=5.3-24.8*

Panju. A., et. al. JAMA. 1998;280(14):1256-1263

Front 291

What is the chance of an MI happening in the presence of ST elevation less than 1 mm?

Back 291

Any ST-segment elevation LR=11.2

Panju. A., et. al. JAMA. 1998;280(14):1256-1263

Front 292

What is the chance of an MI happening in the presence of new T wave inversions?

Back 292

New T-wave inversion LR=2.4-2.8*
Panju. A., et. al. JAMA. 1998;280(14):1256-1263

Front 293

Describe briefly the two mechanisms for acid excretion in the kidneys.

Back 293

In proximal tubule, bicarb is reabsorbed by Na-H exchange (90%). In distal tubule, H+ is secreted by H-ATPase (10%)
Aldo promotes K+ and H+ excretion

Front 294

What is the definition of RTA?

Back 294

Renal tubular acidosis: Defect in either ability to secrete ammonia or hydrogen ions

Front 295

What is the metabolic derangement seen in RTA?

Back 295

All forms characterized by a normal anion gap (hyperchloremic) metabolic acidosis

Front 296

What is the mechanism of RTA 1?

Back 296

Mechanisms: Decreased proton pump (H-ATPase) activity
Increased luminal membrane permeability with backleak of hydrogen ions
Diminished distal tubular sodium reabsorption which reduces the electrical gradient for proton secretion (*hyperkalemia observed)

Front 297

What is the most common cause of RTA1?

Back 297

MCC in adults is Sjögren's syndrome and other hyperglobulinemic

Front 298

What is the serum potassium in RTA1? What is the urine calcium in RTA1?

Back 298

Hypercalciuria due to the effects of chronic acidosis on bone resorption
Hypokalemia (unknown mechanism)

Front 299

What is the mechanism of Type 2 RTA?

Back 299

Type 2 RTA (Proximal): bicarb wasting when plasma bicarb concentration supercedes renal capacity

Front 300

What are the most common causes of RTA2?

Back 300

MCC is multiple myeloma light chain excretion
Fanconi's syndrome: Bicarbonaturia, glucosuria, phosphaturia, uricosuria, aminoaciduria, tubular proteinuria
Acetazolamide (CA inhibitor)
Ifosfamide (anti-cancer tx)
Cystinosis (congenital form of retention of cysteine in different organs and tissues)

Front 301

How do you make the diagnosis of RTA2?

Back 301

Dx: measure urine pH and fractional bicarbonate excretion during a bicarb infusion. Hallmark is a urine pH above 7.5.

Front 302

What is the mechanism of RTA4?

Back 302

Mechanisms: hypoaldosteronism or resistance to action of aldo

Front 303

What is the most common cause of RTA4 in adults? in children?

Back 303

MCC in adults is moderate renal insufficiency e.g. diabetic nephropathy
Children: Adrenal insufficiency, CAH

Front 304

What is the plasma potassium level in RTA4?

Back 304

Hyperkalemia (since aldo cannot excrete it out)

Front 305

How do you make the diagnosis of RTA4? How do you treat?

Back 305

Dx: hyporeninemic hypolaldosteronism
Tx: Fludrocortisone (for ↑K+), restrict K+ in diet, diuretics

Front 306

What's the first step in chronic lower extremity edema?

Back 306

Because bilateral edema may be due to medication, most
commonly a nonsteroidal anti-inflammatory drugs, corticosteroids, or CCB, the first suggestion is to stop the medication.
Blankfield, R. et al Am J Medicine (1998) 105; 192-197

Front 307

Your patient with chronic lower extremity edema comes for evaluation. What determines if you order a TTE or sleep study?

Back 307

Echocardiographic evaluation, including an estimation of pulmonary artery pressure, should be considered for all patients >45 yo with bilateral leg edema. Sleep studies may be appropriate in those who are found to have pulmonary hypertension without an apparent cause.

Blankfield, R. et al Am J Medicine (1998) 105; 192-197

Front 308

Why do African Americans have higher rates of kidney failure than Caucasians?

Back 308

Sequence variations in apolipoprotein L1 (ApoL1) contribute to increased risk of kidney disease in African Americans. Interestingly, ApoL1 variants have also been shown to lyse subspecies of Trypanosoma. The findings that the protective effects of ApoL1 against Trypanosoma are dominant, while the association with renal disease is recessive, support a possible explanation of natural selection.

Genovese et al. Science 2010;329:841-845

Front 309

Is it safe to anticoagulate patients with venous thromboembolism and brain metastases?

Back 309

Tumors with high rates of hemorrhage include thyroid cancer, melanoma, renal cell carcinoma, and choriocarcinoma. Anticoagulation is generally contraindicated in these tumors. However, the majority of metastatic brain tumors (70%) are of breast and lung primary with spontaneous bleeding rates of 1% and 5% respectively. Given the high mortality rate of untreated venous thromboembolism in this population (17-34%), the balance generally favors anticoagulation in patients with low-risk brain metastases.

Gerber et al. J Clin Oncol 2006;24(8):1310-8

Front 310

Is a diagnosis of cancer a contraindication to TPA administration for stroke?

Back 310

Although the original TPA trial stroke published in 1995 (N Engl J Med 1995; 333:1581-1588) and the extended window ECASS III trials published in 2008 (N Engl J Med 2008; 359:1317-1329) do not have cancer as one of the exclusion criteria, it is unknown how many of the patients studied had cancer at the time of TPA administration.

A separate retrospective review looking rTPA for acute stroke at an academic cancer center reported six patients with cancer treated with rTPA . 4 out of 6 had early neurologic recovery, while only 1 of 6 patients suffered minor bleeding as a complication of rTPA.

Graber et al. J Neurooncol 2012;107(3):571-3

Front 311

How do you treat exercise induced asthma?

Back 311

Evidence of low to moderate quality shows that beta2-agonists, both SABA and LABA, when administered in a single dose, are effective and safe in preventing Exercise-induced asthma.

Bonini M, Di Mambro C, Calderon MA, et al. Beta-agonists for exercise-induced asthma. Cochrane Database Syst Rev. 2013 Oct 2;10:CD003564. (Review)

Front 312

Does using gloves and gowns on every single patient in the ICU result in decreased nosocomial infection?

Back 312

The use of gloves and gowns for all patient contact compared with usual care among patients in medical and surgical ICUs did not result in a difference in the primary outcome of acquisition of MRSA or VRE. Although there was a lower risk of MRSA acquisition alone and no difference in adverse events, these secondary outcomes require replication before reaching definitive conclusions.

Harris AD, Pineles L, Belton B, et al. Universal Glove and Gown Use and Acquisition of Antibiotic-Resistant Bacteria in the ICU: A Randomized Trial. JAMA. 2013 Oct 4.

Front 313

What is the mortality benefit of fecal occult blood testing?

Back 313

The effect of screening with fecal occult-blood testing on colorectal-cancer mortality persists after 30 years but does not influence all-cause mortality. The sustained reduction in colorectal-cancer mortality supports the effect of polypectomy.

Shaukat A, Mongin SJ, Geisser MS, et al. Long-term mortality after screening for colorectal cancer. N Engl J Med. 2013 Sep 19;369(12):1106-14.

Front 314

Your OB colleague calls to find out what is the best diabetic medicine. What do you say?

Back 314

Metformin was found to provide adequate glycemic control with lower mean glucose levels throughout the day, less weight gain and a lower frequency of neonatal hypoglycemia. Logistic regression analysis showed that gestational age at diagnosis and mean pretreatment glucose level were predictors of the need for supplemental insulin therapy in women initially treated with metformin.

Spaulonci CP, Bernardes LS, Trindade TC, et al. Randomized trial of metformin vs insulin in the management of gestational diabetes. Am J Obstet Gynecol. 2013 Jul;209(1):34

Front 315

What are the most sensitive and specific findings on CXR for pulmonary TB?

Back 315

Upper lobe infiltrates (pooled diagnostic OR 3.57, 95% CI 2.38-5.37) and cavities (diagnostic OR range 1.97-25.6) were significantly associated with PTB.

Pinto LM, Pai M, Dheda K, et al. Scoring systems using chest radiographic features for the diagnosis of pulmonary tuberculosis in adults: a systematic review. Eur Respir J. 2013 Aug;42(2):480-94.

Front 316

Your febrile neutropenic patient who is stable wants to be kept out of the hospital. What do you do?

Back 316

Based on the present data, oral treatment is an acceptable alternative to intravenous antibiotic treatment in febrile neutropenic cancer patients (excluding patients with acute leukaemia) who are haemodynamically stable, without organ failure, and do not have pneumonia, infection of a central line or a severe soft-tissue infection. Quinolones alone or combined with another antibiotic were used with comparable results.

Vidal L, Ben Dor I, Paul M, et al. Oral versus intravenous antibiotic treatment for febrile neutropenia in cancer patients. Cochrane Database Syst Rev. 2013 Oct 9;10

Front 317

Your patient with a high risk cardiac history needs anti-coagulation and is on Dabigatran. What do you do?

Back 317

Oral DTIs were associated with increased risk of MI. This increased risk appears to be a class effect of these agents, not a specific phenomenon unique to dabigatran or protective effect of warfarin.

Artang R, Rome E, Nielsen JD, et al. Meta-Analysis of Randomized Controlled Trials on Risk of Myocardial Infarction from the Use of
Oral Direct Thrombin Inhibitors. Am J Cardiol. 2013 Sep 25.

Front 318

What is the cardinal symptoms of acute mountain sickness?

Back 318

Headache. Accompanied by nausea, anorexia, dizziness, malaise, sleep disturbance, or a combination.

Front 319

What alititude is usually needed for acute high-altitude sickness?

Back 319

2500 meters. Prevalence and severity increase with increasing altitude (50-85% of unacclimated persons at 4500-5500m)

Front 320

What is the timing of onset of acute high-altitude sickness?

Back 320

Within 6-12 hours after a person ascends to 2500m or higher.

Front 321

What is the clinical marker of high-altitude cerebral edema? What is this diseases timing in relation to ascension?

Back 321

Headache that is poorly responsive to NSAIDs and vomiting. Often associated with truncal ataxia, decreased conciousness, and usually mild fever.
Usually develops after at least 2 days at altitudes above 4000m.

Front 322

What are the clinical features of high-altitude pulmonary edema? What is its clinical onset?

Back 322

Loss of stamina, dyspnea first with exertion followed by rest, dry cough with exertion.

Usually develops 2 or more days after exposure to altitudes above 3000m and is rare in persons at altitudes below 2500-3000m.

Front 323

What is the estimated mortality of persons with high-altitude pulmonary edema? Pathophys?

Back 323

50%. Noncardiogenic pulmonary edema caused by exaggerated hypoxic pulmonary vasoconstriction and abnormally high pulmonary-artery pressure and capillary pressure. This leads to hemorragic capillary leak that secondarily may evoke an inflammatory response.

Front 324

What non-pharmacologic intervention can you offer to minimize the risk of acute altitude sickness?

Back 324

An ascent made after 1 week at an altitude of 2000m or higher, as compared with an ascent from near sea level, reduces both the incidence and severity of acute mountain sickness at 4300m by 50%.

Beidelman, BA et al High Alt Med Biol 2009; 10: 253-60.

Front 325

What prophylactic medication is available for prevention of acute mountain sickness headache?

Back 325

Acetylsalicylic acid 320mg taken three times at 4-hour intervals, starting 1 hour before ascent. Or, ibuprofen at a dose of 600mg three times per day, starting a few hours before ascent to altitudes between 3500 and 5000m.

Front 326

What is the benefit of acetazolamide for acute mountain sickness?

Back 326

The use of acetazolamide was associated with a 44% reduction in the risk of high-altitude illnesses. 125mg twice a day is the minimal effective dose and it should be started one day before the ascent.

Front 327

What are the side effects of acetazolamide use?

Back 327

Acral paresthesia, polyuria, nausea, tiredness

Front 328

Treatment for acute high altitude sickness.

Back 328

Rest, NSAIDs for headache, possibly anti-emetic drugs. Oxygen and acetazolamide are effective. Immediate descent is lifesaving when severe symptoms suggest the onset of high-altitude cerebral edema or pulmonary edema.

Front 329

Treatment for high-altitude pulmonary edema.

Back 329

Rest, descent, Nifedipine ER 30mg BID, Oxygen. No role for diuretics.

Front 330

What is the most commonly affected region of the colon in ischemic colitis?

Back 330

Left colon and sigmoid in 40% of cases.

Front 331

What is the most common symptom of ischemic colitis?

Back 331

Abdominal pain.

Front 332

Describe symptom progression of abdominal pain in ischemic colitis?

Back 332

In patients where the ischaemic damage is localized to the mucosa, it is the afferent nerves of the autonomic nervous system that transmit this visceral pain. Visceral pain is not accurately localized and, when arising from the hindgut (left colon and rectum), it is typically referred to the left lower quadrant and left-flank area. Visceral pain arising from the midgut (right colon) is often referred to the central abdomen. Intestinal hypermotility often adds a crampy or colicky component to the pain. Should the ischaemia become transmural, the patient will experience pain derived from the parietal peritoneum. At that time an examining physician will be able to detect peritoneal signs of guarding and rebound tenderness.

Front 333

Describe the presentation of bleeding in acute mesenteric ischemia?

Back 333

Melena or haematochezia occurs in 15% of cases, and occult blood is detected in at least half of patients.

Front 334

What is D-lactate and what can it be used to detect biochemically?

Back 334

D-Lactate is produced only by bacteria, especially in the colon, as a normal product of bacterial fermentation. Serum baseline levels of D-lactate are very low in healthy humans, probably the e􏰂ect of an intact colonic mucosal barrier. With colonic ischaemia, intestinal permeability increases, allowing D-lactate to enter the circulation.

Front 335

Why is serum lactate a poor marker of intestinal ischemia?

Back 335

Serum lactate levels rise with intestinal ischaemia. However, any and all tissue hypoxia will result in its production and thus it is not a specific marker of intestinal ischaemia. Further degrading its utility is the fact that lactate, produced by the ischaemic gut, is extracted from the portal circulation by the liver. Thus, in the early stage of intestinal ischaemia, serum lactate levels may be normal.

Front 336

What are the findings suggestive of ischemic colitis on CT of Abdomen/ Pelvis?

Back 336

Segmental bowel wall thickening is seen in most cases and can be graded as mild (3±6 mm), moderate (6±12 mm) and severe (>12 mm). In a study of 54 cases of ischaemic colitis, the average wall thickness of the ischaemic area was 8 mm, mild to moderate ascites was present in 37% and intramural pneumotosis was only seen in 6%.

Front 337

Can findings on CT prognosticate the course of ischemic colitis?

Back 337

However, an important finding of this study was that CT findings did not correlate with, nor did they predict, the development of bowel infarction.

Front 338

What is the role of mesenteric angiography in the diagnosis of ischemic colitis?

Back 338

When the disease is thought to involve the left colon, mesenteric angiography may identify evidence of atherosclerotic vascular disease, but it seldom identifies an acute arterial obstruction as the cause of the colonic ischaemia. In cases of non- occlusive ischaemia, by the time the angiogram is performed, blood ̄flow to the colon is usually restored and, thus, the angiogram will have a normal appearance. With suspected right-sided ischaemic disease, there may be a role for angiography, in particular if acute mesenteric ischaemia is suspected. Also, in suspected cases of ischaemic colitis, where colonoscopy fails to identify any evidence of colonic ischaemia, superior mesenteric angiography should be considered to rule out acute mesenteric ischaemia of the small intestine.

Front 339

What percent of patients with non-gangrenous ischemic colitis will go on to develop obstructive ischemic colitis later?

Back 339

Approximately 10% of patients that initially recover from their ischaemic event may present several months later with obstructive symptoms caused by an ischaemic stricture.

Front 340

Which historical factors are responsible for the development of ischemic colitis requiring surgical therapy?

Back 340

In a recent study of 47 patients, co-existing medical diabetes, initial haemodynamic instability and prolonged ileus were found to be predictors for requiring operative management. Profound hypotension at the time of presentation is not only a predictor of the need for surgical intervention, but also has an associated correlation with increased mortality.

Front 341

Ddx Lateral and anterior vaginal wall tenderness

Back 341

Interstitial cystitis, pelvic floor muscle dysfunction (vaginismus), myalgia

Front 342

Ddx: Pain with speculum examination

Back 342

Interstitial cystitis, vaginismus

Front 343

How does methemoglobin affect pulse oximetry?

Back 343

Methemoglobin is an altered state of hemoglobin in which the ferrous (Fe2+) state of iron is oxidized to the ferric (Fe3+) state, resulting in the inability to bind oxygen. Pulse oximetry measures light at 660 nm and 940 nm. The ratio of absorption of methemoglobin is similar to hemoglobin at 660 nm, but is greater at 940 nm. Studies have shown that the Sp02 detected by pulse oximetry decreases with increasing methemoglobin percentages, until the Sp02 reaches a plateau of approximately 85%. As opposed to pulse oximetry, co-oximetry with arterial blood gas provides an accurate oxygen saturation by measuring the oxygen carrying state of hemoglobin.

Haymond et al. Clinical Chemistry 2005;51(2):434-444

Front 344

Is there an association between atrial fibrillation and inflammatory bowel disease?

Back 344

In a large population-based study, there appeared to be an association between inflammatory bowel disease and new-onset atrial fibrillation. Specifically, disease flares and persistent activity were associated with incident atrial fibrillation, with incidence rate ratios of 2.63 and 2.06 respectively, when compared to matched controls. Interestingly, inflammatory bowel disease was not associated with newly incident atrial fibrillation during periods of remission. Inflammation, including atrial myocarditis, has been hypothesized as a potential mechanism to explain this association.

Kristensen et al. Europace. 2013 Oct 9. Epub ahead of print

Front 345

What is the mortality associated with upper GI bleeding?

Back 345

Upper GI bleeding has been estimated to account for up to 20,000 deaths annually in the United States. The incidence rate for upper GI bleeding appears to be, in general, decreasing from 170 per 100,000 in 1998 to 146 per 100,000 in 2006. This is thought to be due to prescription of proton pump inhibitors and efforts to eradicate H pylori infections. Consequently, the number of inpatient deaths attributed to GI bleeding has decreased from 7 per 100,000 in 1998 to 5 per 100,000 in 2006.

El-Tawil et al. World J Gastroenterol 2012;18(11):1154-1158

Front 346

What is empagliflozin?

Back 346

a sodium glucose cotransporter 2 (SGLT2) inhibitor

Front 347

What is the effect of Metoclopramide in pregnancy?

Back 347

Metoclopramide use in pregnancy was not associated with increased risk of major congenital malformations overall, any of the 20 individual malformation categories assessed, spontaneous abortion, or stillbirth. These safety data may help inform decision making when treatment with metoclopramide is considered in pregnancy.

Front 348

You want to prognosticate your patient with pancreatitis. What system do you use?

Back 348

Atlanta 2012 and DBC severity categories accurately reflected clinical outcomes in our cohort and were superior to Atlanta 1992. These novel classification systems can guide the selection of homogeneous patient populations for clinical research and provide an accurate spectrum of disease severity categories in the clinical setting.

Nawaz H, Am J Gastroenterol. 2013 Oct 15.

Front 349

What is the difference between atopic dermatitis and eczema?

Back 349

Eczema and atopic dermatitis (AD) are often used synonymously. The distinction is that eczema can mean inflamed skin from any cause, whereas AD is the relapsing-remitting pruritic rash that occurs at typical sites, mainly the face and skin creases, and is associated with other type I allergic disorders, such as asthma, food allergies, and allergic rhinitis.

Front 350

What is the most common mutation in patients with atopic dermatitis? What are the two types of atopic dermatitis?

Back 350

Mutations in filaggrin, an epidermal-barrier protein, occur in about 15% of patients and are considered major predisposing factors. Controversy surrounds recent proposals that there are 2 types of AD, intrinsic and extrinsic (7). The extrinsic type is described as classical AD that occurs in conjunction with elevated IgE to various airborne and food allergens and is likely to show filaggrin mutation, whereas intrinsic AD is associated with normal IgE levels and a lack of mutated filaggrin.

Front 351

In what age do most patients with atopic dermatitis present?

Back 351

The disorder begins in the first 18 months of life in approximately 65% of patients and persists beyond adolescence in 40%.

Front 352

What items in the history and physical examination suggest atopic dermatitis?

Back 352

Patient must have pruritus in the past 12 months, plus 3 or more of the following:
History of skin-crease dermatitis or cheek dermatitis (in infants)
Personal history of asthma or hay fever (or first-degree relative if < age 4 y)
History of generalized dry skin in past year
Visible skin-crease dermatitis (or dermatitis of the cheeks, forehead, or outer limbs if < age 4 y)
Onset before age 2 years (not used in patients < age 4 y)

Front 353

What elements of the history should clinicians focus on in evaluating patients with AD?

Back 353

Elements of the patient's history that strongly suggest AD are early child- hood onset, generalized dry skin, pruritus and scratching, other family members with AD, and a personal or family history of such allergic disorders as asthma, allergic rhinitis, and food allergies. If treatment has been tried with topical corticosteroids, a full or partial response and subsequent relapse are exceedingly common

Front 354

Rank the following three steroids in order of potency: Fluticasone propionate, lobetasol propionate; Hydrocortisone acetate, Alclometasone dipropionate, Fluocinolone acetonide, betamethasone

Back 354

Highest Potency: lobetasol propionate; betamethasone
Mid-High Potency: Fluticasone propionate
Mid Potency: Fluocinolone acetonide
Low-Mid Potency: Alclometasone dipropionate
Low Potency: Hydrocortisone acetate

Front 355

How should topical steroids for atopic dermatitis be prescribed?

Back 355

Mid-to high-potency corticosteroids in classes 1 to 5 can be highly effective for AD but should be reserved for nonfacial, noninter- triginous skin areas in adults and adolescents. Corticosteroid classes 6 and 7, the lowest-strength non- fluorinated compounds, are recommended for AD in many clinical situations, including the care of young children and treatment of the face, neck, groin area, and skin creases in all age groups.

Front 356

What are the side effects of topical steroids?

Back 356

The more potent the medication, the greater the risk for side effects, in- cluding local acne-like eruptions, skin atrophy, and stretch marks; systemic effects, such as suppression of the hypothalamic-pituitary-adrenal axis (37); osteoporosis; and ocular problems like cataracts and glaucoma that are concerns when treating the eyelids.

Front 357

What are the best approaches to treat and prevent bacterial superinfection?

Back 357

Mupirocin cream or ointment, applied twice daily, can be alternated or layered under corticosteroid preparations on fissured and crusted areas to treat culture-proven localized infection. Studies have shown that AD patients carry these organisms in their nostrils and under the fingernails; these areas should be treated with twice-daily topical applications of mupirocin for 7 to 10 days to re- duce risk for reinfection. Widespread crusted lesions require appropriate oral antibiotic therapy based on bacterial culture and sensitivity results.

Front 358

What are the second-line side effects of the topical calcineurin inhibitors for atopic dermatitis? Tacrolimus and Pimecrolimus

Back 358

The only local side effect of cal- cineurin inhibitors is occasional mild stinging. The prescriber should be aware that these drugs carry an FDA "black box" warning stating that topi- cal use has been associated with rare cases of lymphoreticular and skin can- cer. However, professional task forces of the AAD and the AAAI have dis- puted a causal relationship

Front 359

When do you think about systemic steroids in allergic contact dermtitis?

Back 359

If allergic contact dermatitis involves an extensive area of skin (greater than 20 percent), systemic steroid therapy is often required and offers relief within 12 to 24 hours. 4 Five to seven days of prednisone, 0.5 to 1 mg per kg daily, is recommended. If the patient is comfort able after this initial therapy, the dose may be reduced by 50 percent for the next five to seven days. The rate of reduction of the steroid dosage depends on factors such as the severity and duration of allergic contact dermatitis, and how effectively the allergen can be avoided.

Front 360

How do you make the diagnosis of contact dermatitis?

Back 360

H&P, but also, refer to derm for PATCH testing.

Front 361

You have an asymptomatic patient with chronic urticaria and minimal history and physical exam findings. Whats the next step?

Back 361

CBC w/ diff, UA, ESR, LFTs

Front 362

What are the causes of urticaria and angioedema?

Back 362

Immunologic (Type 1-4 allergy); Non-immunologic (non IgE mediated): physical stimuli, Direct mast cell degranulation (usually drugs e.g. Vanco), Foods containing high amounts of histamines (strawberries, tomatoes, shrimp, lobster, cheese, spinach, eggplant)

Front 363

Your patient develops wheals and swelling immediately or up to 60 min after food ingestion, recent change in diet, ingestion of processed foods. What's your diagnosis?

Back 363

Allergy to foods, preservatives, or food coloring agents.

Front 364

Your patient develops hives after exercising, sun exposure, cold or heat exposure, water exposure, pressure, vibration. What's your diagnosis?

Back 364

Physical or environmental exposure related urticaria or angioedema.

Front 365

Your patient with a history of urticaria and angioedema or isolated angioedema is asking for treatment. What's the next step?

Back 365

1) Prescribe EpiPen
2) Non-sedating H1 antagonist
-may add Hydroxyzine or Diphenhydramine
-may add Leukotriene modifier
-may add oral corticosteroid
-consult with allergy-immunologist

Front 366

What are the initial diagnostic tests for restless leg syndrome?

Back 366

Basic metabolic and ferritin. Lower ferritin is correlated with the probability of RLS. Consider giving iron in patients with RLS and ferritin <50.

Front 367

Your patient with depression and restless leg syndrome is asking for medication, what do you choose?

Back 367

Bupropion (Wellbutrin)

Front 368

What are the criteria for the diagnosis of restless leg syndrome?

Back 368

Urge to move legs usually accompanied or caused by uncomfortable or unpleasant sensation in the legs.
Urge to move or unpleasant sensation begins or worsens during periods of rest or inactivity.
Urge to move or unpleasant sensation partially or totally relieved by movement (such as walking or stretching) as long as activity continues.
Urge to move or unpleasant sensation worse in the evening or night.
Supportive Clinical Features:
-Periodic limb movements
-Positive family history
-Response to dopaminergic therapy

Front 369

Differential diagnosis of restless leg syndrome.

Back 369

Akathisia - internal desire to move (usually on neuroleptics)
Nocturnal leg cramps (palpable tightening of the leg muscles)
Neuropathy
Peripheral vascular disease

Front 370

When should clinicians consider prescription drug therapy for patients with insomnia?

Back 370

When other approaches prove inadequate, prescription drug ther- apy tailored to the underlying cause of insomnia may be warranted. Al- though drug therapy in the short- term is as effective as behavioral interventions, concomitant use of hypnotics and behavior therapy may mitigate the efficacy of the behavioral measures.

Front 371

What are the contraindications to drug therapy in the treatment of patients with insomnia?

Back 371

In general, H1-blocker antihista- mines are not recommended for patients with angina, heart disease, glaucoma, pulmonary disease, or problems with urinating, as well as patients taking some medications. Likewise, natural remedies, such as St. John's wort, may interact ad- versely with prescribed medications.
Patients taking sedative-hypnotic agents should restrict alcohol in- take, or avoid alcohol all together. They must use particular care when driving or using hazardous equipment.
Patients who are pregnant or breastfeeding should avoid hyp- notics. Patients with underlying disorders, such as OSAS, in which hypnotic use can be counterproduc- tive should also avoid them.

Front 372

What measure can you use to prognosticate heart failure patients?

Back 372

A recent study used the Seattle Heart Failure model to analyze patients in the Randomized Evaluation of Mechanical Assistance in Treat- ment of Chronic Heart Failure (REMATCH) trial and con- cluded that patients could be stratified into high, medium, and low risk for L V AD support.

Front 373

What measure can you use to prognosticate mortality after LVAD implantation?

Back 373

Lietz and Miller score. A score >17 confers a high risk of death within 90 days after LVAD.

Front 374

What is the interaction between nutrition and LVAD placement?

Back 374

Conversely, studies have shown that cachexia (a BMI <22 kg/m2) is associated with a high risk for peri-operative death, often due to infection.28,29 Hence, nutrition needs to be improved before LVAD implant (a pre-albumin level >15 mg/dl).

Front 375

What is the association between RV Failure and LVAD placement?

Back 375

RV failure is a leading cause of morbidity and death after LVAD implant due to the inability of the RV to pump sufficient blood through the pulmonary circuit to adequately fill the left heart.

Front 376

How do you calculate RV stroke work index and how is it useful in LVAD patients?

Back 376

Low pre-operative RV stroke work index (RVSWI) has been demonstrated to predict prolonged inotropic use after pulsatile LVAD implant, supporting the role of RVSWI as a predictor of RV dysfunction.37 In 1 study, inotropic sup- port 􏰀14 days post-operatively was required in 38% of patients with a RVSWI <600 mm Hg ml/m2 compared with 29% of patients with a RVSWI 600 to 900 mm Hg mL/m2, and only 3% with a RVSWI >900 mm Hg mL/m2.38 RVSWI provides a quantitative measure of the ability of the RV to generate pressure and flow and is calculated using this formula:
RVSWI mm Hg ml ⁄ m2 = {[meanPAP(mmHg) - mean CVP (mmHg) ] x SV (ml)} ⁄ BSA (m2)

Front 377

What valvulopathy is most concerning pre-op prior to LVAD placement?

Back 377

Severe tricuspid regurgitation also can be associated with early post-opera- tive RV failure. Some have advocated repair of the tricuspid regurgitation at the time of LVAD implant if its severity is judged to be more than moderate, either pre-operatively or intraoperatively by echocardiogram.

Front 378

What is the difference in osmolar and anion gap between methanol, ethylene glycol, and isopropyl alcohol?

Back 378

Methanol and ethylene glycol present with high anion gap metabolic acidosis and high osmolar gap (OG), whereas isopropanol presents with high osmolarity alone.

Front 379

What is the minimal lethal dose for ethylene glycol in adults?

Back 379

Minimal lethal dose of EG for an adult is 1.0 to 1.5 mL/kg or 100 mL.

Front 380

Metabolism of ethylene glycol poisoning?

Back 380

Liver metabolizes 80% of the absorbed dose of EG,
and proximal tubules reabsorb 80% of filtered EG. Twenty
percent of the EG is excreted unchanged by the kidneys.7 EG is
oxidized by alcohol dehydrogenase to glycolaldehyde and then
to glycolic acid. The rate-limiting step is the slow conversion of
glycolic acid to glyoxalic acid.

Front 381

Clinical presentation of ethylene glycol poisoning?

Back 381

Any order and one or more may be absent.
(1) neurologic - acidosis worsens with CNS deposition of oxalate crystals = altered MS, hypotonia, hyporeflexia, and occasionally, seizures, and meningismus
(2) cardiopulmonary - hyperventilation, HF, shock/ death
(3) renal - oliguria, flank pain, ATN, renal failure, and rarely bone marrow suppression

Front 382

What is a normal osmolar gap? What is the problem with calculating osmolar gap in ethylene glycol poisoning?

Back 382

Normally, the value of the gap is 10 to 15 mOsm/kg.
Early in the course of ingestion, EG contributes to
significant OG, but as metabolites start forming, the OG disappears and the anion gap increases. This indicates that OG, as a measure of severity of poisoning, is only valuable early in the course of intoxication.

Front 383

In general, what is the treatment for ethylene glycol poisoning?

Back 383

Dialysis or fomepizole or ethanol, which competitively bind to alcohol dehydrogenase.

Front 384

When do you give an antidote for ethylene glycol poisoning?

Back 384

EG >20 mg/dL
Recent (hours) ingestion of >100mL of EG PLUS osmolal gap 10 mOsm/L
History or strong clinical suspicion of ethylene glycol poisoning and at least 2 of the following criteria:
1) Arterial pH <7.3
2) Serum bicarbonate <20 mEq/L
3) Osmolal gap >10 mOsm/L
4) Urinary oxalate crystals present

Front 385

When do you choose dialysis for ethylene glycol poisoning?

Back 385

Deteriorating clinical status despite supportive therapy,
metabolic acidosis (arterial pH <7.25-7.30) and/or
Acute kidney injury with a serum creatinine 3.0 mg/dL (265
mmol/L) or increase in serum creatinine by 1.0 mg/dL
(90 mmol/L), or
Acid-base/electrolyte abnormalities unresponsive to standard
treatment

Front 386

How do you dose ethanol for ethylene glycol poisoning?

Back 386

Ethanol can be given intravenously as 10% ethanol
diluted in D5W (10 g of ethanol/100 mL of solution). The
loading dose of ethanol is 0.6 to 0.7 g ethanol/kg (7.6 mL 10%
ethanol/kg), and the maintenance dose is 66 mg ethanol/kg/hr
(0.83 mL 10% ethanol/kg/hr) for nondrinkers and 154 mg
ethanol/kg/hr (1.96 mL 10% ethanol/kg/hr) for alcoholics, although the use of ethanol is not approved by Food and Drug
Administration in EG detoxification.

Front 387

How do you dose fomepizole for ethylene glycol poisoning?

Back 387

Fomepizole is given at a loading dose of 15 mg/kg
followed by 10 mg/kg every 12 hours for 2 days. After 48
hours, dose should be increased to 15 mg/kg every 12 hours
until EG level is 20 mg/dL and the patient is asymptomatic
with a normal pH.

Front 388

What is the toxic dose of methanol?

Back 388

The lethal dose of pure methanol is estimated to be 1 to
2 mL/kg; permanent blindness and death have been reported
with as little as 0.1 mL/kg (6-10 mL in adults).

Front 389

How is methanol metabolized?

Back 389

Methanol is metabolized in liver. Toxic metabolites of
methanol, resulting from oxidation of methanol, contribute to
the majority of toxicity rather than methanol itself. Methanol is oxidized to formaldehyde by alcohol dehydrogenase. Formaldehyde in the presence of formaldehyde dehydrogenase is oxidized to formic acid, which is the major toxic metabolite of methanol.

Front 390

Why is methanol so bad?

Back 390

Methanol is metabolized to formic acid in the liver which inhibits cytochrome C oxidase activity in mitochondria, thus preventing oxidative metabolism

Front 391

When is the onset of symptoms after methanol poisoning?

Back 391

Depending on the coingestion of ethanol, onset of symptoms ranges from 40 minutes to 72 hours with an average of 24 hours.

Front 392

What are the clinical features of methanol poisoning?

Back 392

Early stages of methanol intoxication are mild and transient, manifesting as mild euphoria, inebriation, and drowsiness, followed by a latent interval phase lasting from 6 to 30 hours during which period metabolism of methanol occurs. Sensorium remains essentially clear, with blurred vision and headache as CNS symptoms. GI symptoms such as nausea, vomiting, and abdominal pain result from pancreatitis. Myoglobinuria is a rare complication of methanol poisoning, which can lead to acute kidney injury, but the diagnosis can be complicated by the interference of serum creatinine measurements with methanol.

Front 393

When do you think about methanol poisoning?

Back 393

Methanol overdose should be considered in patients presenting with altered mental status with visual disturbances, abdominal pain with high anion gap metabolic acidosis, and increased OG in addition to the other underlying causes of increased anion gap and OG

Front 394

When you suspect methanol poisoning, what other alcohols do you send for?

Back 394

measure methanol and ethanol and ethylene glycol levels

Front 395

Supportive care for methanol/ ethanol/ ethylene glycol ingestion?

Back 395

Folic acid supplementation plays an important role in the
management of methanol toxicity. Thiamine and multivitamins
should be administered to patients with associated ethanol
ingestion. Other supportive measures include intravenous fluids
and antiseizure medications for control of seizures.

Front 396

What are the antidotes for methanol poisoning and when should they be administered?

Back 396

Ethanol and fomepizole should be administered rapidly as soon as methanol ingestion is suspected to prevent the formation and accumulation of formate. Administration of fomepizole is preferred to ethanol for many reasons. It is easier to administer and has a longer duration of action, whereas ethanol dosing is complex and is associated with errors, and ethanol should be dosed for every hour compared with every 12 hours administration of fomepizole. There is no associated CNS depression with fomepizole compared with ethanol administration.

Front 397

How long do you dose ethanol or fomepizole for?

Back 397

Antidotes should be administered until the symptoms resolve or metabolic acidosis is resolved or methanol concentration is 20 mg/dL.

Front 398

When do you choose antidotes for methanol poisoning over hemodialysis?

Back 398

Documented plasma methanol concentration 0.20 mg/dL
(200 mg/L), or Documented recent history of ingesting toxic amounts of methanol and osmolal gap >10 mOsm/kg, or
History or strong clinical suspicion of methanol poisoning and
at least 2 of the following criteria
Arterial pH <7.3
Serum bicarbonate <20 meq/L (mmol/L)
Osmolal gap >10 mOsm/kg H2O

Front 399

When do you choose hemodialysis for methanol poisoning over antidotes?

Back 399

Serum methanol levels of 50 mg/dL or Severe metabolic acidosis (pH 7.25 to 7.30) or Visual changes, dose of ingested methanol 30 mL, seizures, and deteriorating clinical status despite intensive supportive therapy, renal failure, or electrolyte abnormalities not responsive to standard therapy

Front 400

Your patient with methanol poisoning completed hemodialysis and his methanol level is <25. Can he be discharged?

Back 400

Close monitoring of serum osmolality and electrolytes should be continued every 2 to 4 hours for 12 to 36 hours after hemodialysis because methanol redistributes resulting in rebound levels.

Front 401

What are the toxic plasma levels of isopropyl alcohol?

Back 401

Isopropanol concentrations of 150 mg/dL produce coma and hypotension, and levels of 200 mg/dL are incompatible with life.

Front 402

What is the metabolism of isopropyl alcohol?

Back 402

Isopropanol is metabolized to acetone by liver, but unlike methanol and EG, the toxic effects are mediated by isopropanol rather than its metabolite.

Front 403

Symptoms of isopropyl alcohol poisoning?

Back 403

Symptoms of isopropanol intoxication usually start within 30 minutes of ingestion. Symptoms range from GI side effects such as nausea, vomiting, abdominal pain, gastritis, and hematemesis to CNS side effects, including headache, dizziness, confusion, stupor, and coma. As a result of profound CNS depression, patients may lie on extremities for prolonged periods, resulting in rhabdomyolysis, myoglobinuria, and acute renal failure.40 Severe intoxication is associated with hypotension, coma, seizures, and death.

Front 404

Diagnosis of isopropyl alcohol poisoning?

Back 404

Isopropanol poisoning can be diagnosed in patients with normal acid-base parameters, hyperosmolarity, and positive nitroprusside reaction in urine and/or blood. Hyperosmolarity is the most common laboratory abnormality associated with isopropanol poisoning.

Front 405

Treatment of isopropyl alcohol poisoning?

Back 405

Supportive measures are generally sufficient if patient is not comatose or hypotensive. Some studies suggest that isopropanol levels between 150 and 200 mg/dL are associated with increased mortality,6,42 whereas in others, blood levels of 400 mg/dL are associated with poor outcome.40 It is reasonable to initiate hemodialysis if the patient presents with hypotension and coma or blood isopropanol levels of 200 mg/dL.

Front 406

What is the definition of subclinical hyperthyroidism?

Back 406

when a low serum TSH level is associated with serum T4 and T3 levels that are within the population reference range. Usually has nothing to do with symptoms. Sxs may or may not be present in subclinical hyperthyroidism

Front 407

Who should be screened for hypo-/hyperthyroidism?

Back 407

1) diffuse or nodular goiters
2) Type 1 DM and autoimmune diseases
3) Family histories of hyperthyroidism or hypothyroidism.
4) Medications: amiodarone (4, 5), alpha-interferon (6), interleukin-2 (7), lithium (8), and iodide (9)
5) osteoporosis, supraventricular tachycardia, or atrial fibrillation
6) All women over age 50 (hyperthyroidism)
7) Head and neck irradiation

Front 408

Anterior neck pain, malaise, fever, and sore throat

Back 408

subacute thyroiditis

Front 409

TSH, T3, and T4 are all consistent with hyperthyroidism and you do NOT suspect Graves (no eye or skin signs). Whats the next step?

Back 409

The radioiodine uptake (RAIU) is the most useful additional diagnostic test and should be ordered whenever the presentation is not diagnostic of Graves disease. Hyperthyroidism associated with high RAIU usually results from 1 of 3 disorders: Graves disease, toxic multinodular goiter, or a toxic adenoma.

Front 410

Describe the thyroid scan results for Graves, Toxic Goiter, and Toxic Adenoma.

Back 410

Graves disease shows diffuse isotope uptake, toxic multinodular goiter shows patchy uptake, and a toxic adenoma shows uptake only in a single nodule.

Front 411

Differential diagnosis of hyperthyroid-like states?

Back 411

infection, sepsis, anxiety, depression, the chronic fatigue syndrome, atrial fibrillation of other causes, and pheochromocytoma

Front 412

Why methimazole over PTU?

Back 412

Both agents are generally quite effective (21), but methimazole should be used because of the potential for hepatic failure with PTU

Front 413

How long do you treat hyperthyroidism for?

Back 413

The optimal duration of methimazole therapy is usually 12-18 months, after which it is tapered or discontinued if the patient is asymptomatic and the TSH level is normal

Front 414

Your patient is about to go for iodine ablation, when do you stop the pre-op prophylactic methimazole?

Back 414

Drugs used for this purpose should be discontinued 7 days before I-131 treatment to prevent them from reducing the effectiveness of the treatment.

Front 415

When do you choose PTU over methimazole for hyperthyroidism?

Back 415

use methimazole instead of PTU, except in thyroid storm, cases of methimazole allergy, and in pregnant women in the first trimester (causes choanal atresia and scalp aplasia)

Front 416

What are the risk factors for agranulocytosis in patients taking meds for hyperthyroidism?

Back 416

Agranulocytosis is a potentially lifethreatening disorder that occurs with both drugs in about 0.2%-0.4% of patients (33, 34), most often within the first few months of treatment; it occurs more commonly in patients receiving high doses (>40 mg/d) of methimazole (35, 33, 36) but is not dose-related in patients taking PTU (35). PTU also causes more antineutrophil cytoplasmic antibody- positive vasculitis (37, 38).

Front 417

What are the side effects of I-131 treatment?

Back 417

Most patients become hypothyroid within 3-6 months of I-131 therapy. Sialadenitis is an occasional side effect from uptake by the salivary glands. Worsening of preexisting Graves orbitopathy is now a well recognized potential complication of I-131 treatment (19, 40-43).

Front 418

What is the treatment decision that needs to be made in patients with Graves oritopathy?

Back 418

Patients with mild orbitopathy can receive I-131 but may benefit from pretreatment with glucocorticoids. Patients with moderate to severe orbitopathy should choose another option

Front 419

What is the RAIU in subclinical hyperthyroidism?

Back 419

The RAIU is typically within the reference range, and thyroid scan findings are consistent with the underlying cause

Front 420

When do you treat subclinical hyperthyroidism?

Back 420

TSH levels <0.1 mU/L or those who are convincingly symptomatic should be treated (48, 49). Debate on management of patients with levels ≥0.1 mU/L but that are still lower than the reference range continues

Front 421

Your patient has a TSH of 0.2 but T3 and T4 level that are normal. They complain of fatigue and difficulty sleeping. What do you do?

Back 421

When patients with subclinical hyperthyroidism have symptoms that may be caused by hyperthyroidism but are too vague for the clinician to be confident about their cause, some experts recommend starting an antithyroid medication and then deciding whether to continue based on whether symptoms improve as the TSH level becomes normal.

Front 422

What is the cardinal manifestation of thyroid storm?

Back 422

Fever >102° F is the cardinal manifestation of this condition.

Front 423

In what age groups are thyroid nodules most likely to be malignant?

Back 423

Nodules in persons younger than 20 years or older than 70 years have an increased risk of malignancy.

Front 424

At what size do you biopsy thyroid nodules?

Back 424

more recent recommendations are to biopsy only those larger than 1 cm.

Front 425

When do you monitor thyroid nodules?

Back 425

Nodules 1 cm or smaller may be followed with serial ultrasonography.

Front 426

You detect a 2cm thyroid nodule on palpation, TSH is low and RAIU shows it is hyperfunctioning. What do you do?

Back 426

Radioactive iodine 131 ablation is the first-line treatment for hyperfunctioning thyroid nodules.

Front 427

Should clinicians screen pregnant women for hypothyroidism?

Back 427

Screening as part of a prepregnancy or early pregnancy evaluation remains controversial. Prospective screening and outcome studies have reported that pregnant women with subclinical hypo-thyroidism are 3 times more likely to have placental abruption and 2 times more likely to have a preterm delivery (10), that perinatal intraventricular hemorrhage and respiratory distress syndrome occur more often in infants of women with subclinical hypothyroidism

Front 428

How do you choose the initial dose of synthroid?

Back 428

In most adults 1.6 mcg/kg (IBW)/ day. Always titrate every 6 to 8 weeks based on the TSH.
But, patients older than 60 years should be treated with an initial LT4 dose of 25 to 50 μg/d and dose increases in 12.5- to 25-μg increments every 6 to 8 weeks until the desired dose is reached.

Front 429

What are the indications for treating subclinical hypothyroidism?

Back 429

Patients who have serum TSH levels higher than 10 mU/L should be strongly considered for LT4 treatment
(8, 9). Patients with serum TSH levels of 5 to 10 mU/L should also be considered for LT4 treatment if they have symptoms suggestive of thyroid hormone deficiency, elevated serum LDL cholesterol levels, goiters, or positive antithyroid antibodies

Front 430

When someone is infected with TB, when are they most likely to develop active disease? What is their lifetime risk of developing active disease?

Back 430

The greatest risk of progres- sion from LTBI to active tuberculosis occurs in the first two years after infection, when about one half of the 5 to 10 percent lifetime risk occurs.

Front 431

Your patient with Latent TB for many years suddenly develops active TB with fevers and night sweats. What is the differential of risk factors for the development of active disease?

Back 431

This risk is increased in children younger than four years; persons with HIV infection, diabetes, and other chronic conditions; those using immunosuppressant medications; and those with apical fibronodular changes on chest radiography. As well as TNF-alpha inhibitors.

Front 432

In whom do you screen for Latent TB?

Back 432

The decision to screen for tuberculosis is a decision to treat, regardless of BCG status. LTBI screening is effective in two groups of per- sons: those at risk of contracting M. tuberculosis and those at risk of progressing from LTBI to active tuberculosis.

Front 433

Your IGRA assay comes back indeterminate, what do you do?

Back 433

Indeterminate results require follow-up testing using IGRA or TST only if the patient is at increased risk of infection.

Front 434

Your patient recently was released from prison, where he had close contact with a fellow inmate that had TB. When do you screen him and how long do you treat?

Back 434

If a patient has had recent close contact with a person with active tuberculosis but is still in the 12-week window where TST may be negative, immediate LTBI treatment should be considered if the patient is at high risk of progression to active tuberculosis or has increased susceptibility to disease. A repeat TST should be performed 12 weeks after contact has ended, and treatment should be continued if the TST result is positive, or discontinued if the result is negative.

Front 435

Your HIV-positive patient recently was released from prison, where he had close contact with a fellow inmate that had TB. When do you screen him and how long do you treat?

Back 435

Persons who are immunocompromised, including those with HIV infection, who had contact with individuals with active tuberculosis should continue treatment for LTBI, even if PPD performed 12 weeks after contact is negative.

Front 436

How do you treat LTBI in pregnancy?

Back 436

In pregnant women, a six- to nine-month course of INH may be delayed until after delivery, unless there is increased risk of pla- cental infection or progression to active tuberculosis (e.g., immunocompromising conditions, recent M. tuber- culosis infection).

Front 437

A young child being treated for LTBI with INH. Do you give him Pyridoxine?

Back 437

Routine use of pyridoxine in children taking INH is not recommended, except if the child is symptomatic, breastfeeding, or con- suming a diet likely to be deficient in pyridoxine

Front 438

How often do you monitor patients on INH therapy?

Back 438

Monthly history and physical for signs/ symptoms of hepatitis. LFTs every

Front 439

At what level of LFT abnormality do you discontinue INH?

Back 439

Most experts recommend discon- tinuing INH if transaminase levels are greater than three times the upper limit of normal in symptomatic patients or five times the upper limit of normal in asymptomatic patients.

Front 440

Is there evidence to support the use of oral acetylcysteine for the prevention of contrast-induced neuropathy?

Back 440

The largest trial to address this question, the Acetylcysteine for Contrast-Induced Nephropathy trial (ACT) randomized 2308 patients undergoing some form of angiography to acetylcysteine 1200mg orally twice daily for two doses prior to the procedure and two doses after versus matched placebo. They found no difference in incidence of nephropathy, need for dialysis, mortality or any other adverse effect, overall or in any subgroup. The investigators also did a brief meta-analysis showing that the high quality trials previously performed to address that question were concordance with their results.

ACT Investigators. Circulation 2011;124(11):1250-9

Front 441

What is the risk of Clostridium difficile incurred by fluoroquinolones?

Back 441

A 2003 VA study done in Maryland showed that fluoroquinolone use was associated with an odds ratio of 12.7 of developing C. difficile which is significantly higher than clindamycin at 2.2. An association was also described in a more recent VA study in 2005 between fluoroquinolones and an increased risk for NAP-1 strains, which incurred additional morbidity due to increased virulence.

McCusker et al. Emerg Infect Dis 2003;9(6):730-733

Front 442

What is the evidence for duration of dual antiplatelet therapy following implantation of drug-eluting stents?

Back 442

A recent study (OPTIMIZE) published in JAMA looked at differing durations of dual antiplatelet therapy (DAPT) in patients receiving zotarolimus-eluting stents. 3,119 patients were randomized to 3 months vs. 12 months of DAPT. The primary endpoint of death, MI, stroke or major bleeding was similar at one year between both groups (6% vs. 5.8%). Notably, however, the study had a lower than expected event rate (expected 9%, actual 6%) than anticipated and may have resulted in insufficient powering of the study.

Feres et al. JAMA. Published online October 31, 2013

Front 443

How long does HPV have to infect the cervix for in order to cause cancer?

Back 443

persistent infection at 1 year and 2 years strongly predicts subsequent risk of cervical intraepithelial neo- plasia (CIN) 3 or cancer regardless of age

Front 444

Does HPV persist longer in older women above the age of 30?

Back 444

Newly acquired HPV infection appears to have the same low chance of per- sistence regardless of age in women aged 30 years and older. However, HPV infection detected in women older than 30 years is more likely to reflect persistent infection.

Front 445

When do you immunize women against HPV?

Back 445

Both the Advisory Committee on Immunization Practices (ACIP) of the Centers for Dis- ease Control and Prevention and the American College of Obstetricians and Gynecologists recommend administra- tion of the vaccine to females aged 9-26 years

Front 446

At what age do you begin Cervical Cancer Screening?

Back 446

Cervical cancer screening should begin at age 21 years. Women younger than 21 years should not be screened regardless of the age of sexual initiation or the presence of other behavior-related risk factors.

Front 447

In what demographic group of women do you have to think about more frequent Pap testing?

Back 447

Women with cervical cancer and those who have HIV infection, are immunocompromised, or were exposed to diethylstilbestrol in utero.

Front 448

What is one modifiable risk factor for breast cancer?

Back 448

Counseling women to limit alcohol, lose weight, and exercise are probable opportunities for decreasing breast cancer risk, but this has not been tested in randomized trials.
Women who consume 2 or more alcoholic drinks per day have a 21% higher risk for breast cancer than nondrinkers (12).

Front 449

What are the most serious side effects of Tamoxifen?

Back 449

When compared with placebo, tamoxifen is associated with an increased risk for endometrial cancer, with an RR of about 2. It is also associated with cataracts and thromboembolic disease

Front 450

What are the serious and common side effects of Raloxifene?

Back 450

Compared with placebo, raloxifene does not seem to be associated with endometrial cancer risk (Table 1). Raloxifene is associated with venous thromboembolism with an RR less than 2. Raloxifene patients had a borderline increased risk for fatal stroke in 1 placebo-controlled trial but had no significant increase in the meta-analysis of 2 trials. The most prominent quality-of-life is- sues with raloxifene are hot flashes and peripheral edema.

Front 451

When should clinicians choose from among the medications available for chemoprevention of breast CA?

Back 451

Clinicians should generally limit consideration of chemoprevention to women with an increased risk for breast cancer, based on genetic status, pathologic diagnosis, family history, or a 5-year Gail score of 1.66% or greater

Front 452

What are the diagnostic criteria for IgG4 related diseases?

Back 452

IgG4 related diseases are a broad spectrum of systemic sclerotic diseases, affecting multiple organ systems. IgG4 levels are neither sensitive nor specific for IgG4-related disease. Clinical suspicion must be high and the cornerstone of diagnosis lies within the pathology found on biopsy. Classic pathology includes lymphoplasmocytic IgG4 positive infiltrate, storiform fibrosis, and eosinophils.

Stone et al. NEJM 2012;366:539-551

Front 453

What are the new guidelines for cholesterol management?

Back 453

Four risk groups are identified and targeted with various intensities of statin treatment. The groups are (1) patients with clinical atherosclerotic cardiovascular disease; (2) patients over 21 with LDL-cholesterol greater than 190 mg/dL; (3) patients with diabetes with an LDL between 70 and 190 mg/dL; (4) patients with a 10-year risk of atherosclerotic cardiovascular disease greater than 7.5% using the pooled cohort equation. Although the changes in statin treatment thresholds are the most widely reported changes in the guidelines, lifestyle modification remains an integral aspect of the treatment of dyslipidemia.

Stone et al. Circulation. 2013 Nov 12. [Epub ahead of print]

Front 454

Which bacteria are most likely to cause parapneumonic effusions?

Back 454

The vast majority of organisms thought to be responsible for a parapneumonic effusion or empyema are the same as those causing the pneumonia. However, putrid odor of empyema fluid is considered diagnostic of anaerobic infection. Fusobacterium nucleatum, Prevotella species, Peptostreptococcus, and Bacteroides fragilis have been cultured in 36-76% of human empyemas. The high incidence of anaerobic infection in empyema probably results from the indolent nature of these pneumonias, which permits pleural penetration of bacteria before antibiotics are instituted.

Kawanami et al. Chest 2011;139(3):600

Front 455

What are the screening guidelines for patients with cirrhosis?

Back 455

The current practice guidelines recommend ultrasound surveillance every 6 months, without AFP, given the poor sensitivity and specificity. The 6 month interval is a function of the tumor growth rate, not the risk; therefore higher risk patients do not need more frequent screening.

Bruix et al. Hepatology 2010;53(3):1020-1035

Front 456

How has the implementation of electronic medical records affected medication errors?

Back 456

Prior to the implementation of electronic medical records, a key theme in inpatient adverse medication events was impaired physician access to drug and patient related information, leading to errors at the medication ordering stage. Electronic medical records and clinical decision support have been shown to reduce the incidence of adverse medication errors by as much as 50%. However, electronic medical records introduce new forms of error, such as unintended discontinuation of medications, wrong patient orders, and alert fatigue.

Koppel et al. JAMA 2005;293(10):1197-203

Front 457

In 2009, the U.S. Food and Drug Administration issued a black box warning for varenicline regarding neuropsychiatric events. Is there any evidence of this?

Back 457

No evidence that varenicline is associated with adverse neuropsychiatric events.

Gibbons RD, Mann JJ. Varenicline, Smoking Cessation, and Neuropsychiatric Adverse Events. Am J Psychiatry. 2013

Front 458

Is there any increased risk of ovarian cancer and breast cancer associated with oral contraceptive (OC) use among women at elevated risk owing to mutations in BRCA1/2 or a strong family history?

Back 458

Our analyses suggest that associations between ever use of OCs and ovarian and breast cancer among women who are BRCA1 or BRCA2 mutation carriers are similar to those reported for the general population.

Moorman PG, Havrilesky LJ, Gierisch JM, et al. J Clin Oncol. 2013 Oct 21.

Front 459

What are the common side effects of PDE4 inhibitors in COPD?

Back 459

PDE4 inhibitors like roflumilast in particular was associated with weight loss during the trial period and an increase in insomnia and depressive mood symptoms.

Chong J, Leung B, Poole P. Phosphodiesterase 4 inhibitors for chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2013 Nov 4;11

Front 460

You decide to treat a patient with acute migraine with sumatriptan and promethazine. What are the side effects to be aware of?

Back 460

The only significant drug-related adverse events reported in >/=15% of patients in any treatment group were somnolence (32.2% and 7% in the SPr and SP groups, respectively, P < .001), extrapyramidal symptoms (4.3% and 0%, P = .05), and nausea (1% and 8%, P = .03).

Asadollahi S, Heidari K, Vafaee R, et al. Promethazine Plus Sumatriptan in the Treatment of Migraine: A Randomized Clinical Trial. Headache. 2013 Nov 1.

Front 461

Are the antibodies that cause thrombocytopenia the same as the ones that cause anemia in Evans Syndrome?

Back 461

Evans Syndrome, first described by Evans and Duane in 1949, refers to the combination of Coombs-positive warm autoimmune hemolytic anemia and immune thrombocytopenia (ITP). The syndrome can be primary or associated with systemic lupus, immune disorders, lymphoproliferative disorders or immunodeficiencies. The antibodies that cause hemolysis are different from those that cause platelet destruction. Those causing hemolysis are directed against a base protein portion of the Rh blood group, while those that destroy platelets are frequently directed against platelet GPIIb/IIIa.

Michel et al. Blood 2009;114(15):3167

Front 462

Does the mode of anesthesia influence perioperative cardiac complications for non-cardiac surgeries?

Back 462

Although common sense may dictate that the increased hemodynamic shifts of general anesthesia would lead to a greater incidence of perioperative cardiac complications, controlled trials and meta-analyses have generally not supported this theory. A study randomizing 100 patients scheduled for elective vascular reconstruction of the lower extremities to either epidural or general anesthesia showed no difference in cardiac outcomes out to six months. This was mirrored in similar studies evaluating 229 patients undergoing elective abdominal aortic aneurysm repair and 186 patients undergoing elective carotid artery surgery, all randomized to local or general anesthesia. A large meta-analysis of 24,716 patients who underwent carotid endarterectomy also showed no difference in cardiovascular complications based on anesthesia type.

Schechter et al. Surgery 2012;152(3):309-14

Front 463

Does a chloride-restrictive (vs. chloride-liberal) intravenous fluid strategy reduce the incidence of acute kidney injury in critically ill patients?

Back 463

A prospective, open-label, study of 1533 patients in Australia were selected to receive either restrictive chloride strategy or usual care, showed that in a chloride restricted group the incidence of acute kidney injury was 8.4% (95% CI, 6.4%-10%; n = 65) vs 14% (95% CI, 11%-16%; n = 105) in a chloride liberal group. The use of renal replacement therapy was also decreased in a chloride restrictive group (odds ratio, 0.52 [95% CI, 0.33-0.81]; P = 0.004). There were no differences in hospital mortality.

Yunos et al. JAMA 2012;308(15):1566-72

Front 464

What are the side effects of K2?

Back 464

K2 is a synthetic cannabinoid that does not appear on routine urine toxicology screens. In case reports of young healthy patients, K2 has been associated with myocardial infarctions (MI). Marijuana has been shown to be a rare cause of MI, with a 4.8 increase in risk of MI in the hour after smoking marijuana, thought to be due to its vasoconstrictor effect. Given K2 has a higher binding affinity than marijuana for the cannabinoid receptor, a vasoconstrictor effect may be the mechanism of K2 causing MIs.

Mir et al. Pediatrics 2011;128:000

Front 465

What is the most common adverse event within 30 days of implantation of a left-ventricular assist device (LVAD)?

Back 465

Following implantation of an LVAD, bleeding is the most common adverse event. Within 30 days, bleeding from the mediastinum is the most common. After 30 days, gastrointestinal bleeding is most common. The proposed mechanism is an acquired von Willebrand factor. One mechanism is that the shear stress from the LVAD is similar to the shear stress from severe aortic stenosis. The high shear stress promotes vWF proteolysis by the metalloproteinase, ADAMTS13, leading to a decrease in multimer size. One trial of 79 patients with a Heartmate II LVAD showed that all patients had decreased or absent vWF multimers, which normalized after the patient received a heart transplantation.

Suarez J. et al. Circulation 2011; 4:779-784

Front 466

What is the prognostic significance of an elevated ANA in patients with malignancy?

Back 466

There have been conflicting results of the prognostic implications of the ANA level in malignancy. In patients with small cell lung and colon cancer who have positive ANA, there has been a significant trend toward more favorable prognosis. While in breast cancer, a positive ANA is associated with recurrent disease. In lymphoma, elevated ANA levels have been attributed to treatment. In one study, close to 20% of the patients with lymphoma had positive ANA with a titer of 1:60 prior to treatment, most frequently found in patients with mantle and follicular lymphoma. Only 28% of these patients actually had any clinical signs of autoimmune disease implying a separate pathophysiology causing an elevated ANA.

Guyomard et al. British Journal of Haematology;123:90-99

Front 467

Does the duration of preoperative beta blockers impact outcomes following noncardiac surgery?

Back 467

A recent retrospective cohort study of 48,103 patients receiving preoperative beta blockers for major elective noncardiac surgery assessed the rates of mortality based upon when beta blockers were initiated. The study found those who started beta blockers 1-7 days preoperatively had an increased 30 day risk of mortality (OR: 1.49 [1.03-2.16]) whereas those having started therapy 8-30 days before and >31 days before did not incur such a risk. These findings suggest that beta blockers should be started at least more than a week prior to undergoing elective noncardiac surgery.

Wijeysundera et al. Can J Cardiol 2013 Oct 24.

Front 468

Is there any benefit to the elective opening of a totally occluded coronary artery?

Back 468

The Occluded Artery Trial (OAT) examined this question among 2201 patients without severe inducible ischemia, rest angina, class III-IV heart failure, or triple-vessel disease who were found to have a total occlusion of their infarct-related artery (IRA) > 24 hours after myocardial infarction. These patients were randomized to percutaneous coronary intervention (PCI) of their IRA versus medical therapy alone. In the primary composite endpoint of death, reinfarction, or class IV heart failure, no significant differences between groups were found after a median of 6 years of follow-up. Although angina was decreased early on in the PCI group, this difference did not persist.

Hochman et al. Circulation 2011;124(21):2320-8

Front 469

What is the utility of N-acetylcysteine (NAC) in patients with non-acetaminophen-induced hepatic failure?

Back 469

One study from the Journal of Gastroenterology was a prospective, double-blind trial of acute liver failure without acetaminophen toxicity. 173 patients were enrolled and randomized to NAC (n=81) or placebo (n=92). Primary outcome was number of patients surviving at 3 weeks. Results showed a trend to increased overall survival (70% in NAC vs. 66% in the placebo group, P=0.28) and a significantly increased transplant free survival with NAC (40%) vs. placebo (27%) (P=0.43).

Lee et al. Gastroenterology 2009;137(3):856-864

Front 470

Is there a sustained mortality benefit with Fecal Occult Blood Testing (FOBT) screening after 30 years?

Back 470

FOBT is a common modality used by many primary care physicians to screen patients for colorectal cancer. In a randomized control study published by Shaukat et al, 46,551 patients between 50 to 80 years of age were assigned to usual care (control), annual FOBT, or biennial FOBT between 1976-1982 and 1986-1992. Participants were followed for a reduction in colorectal cancer mortality and all-cause mortality. Within a follow up period of 30 years, it was shown that both annual FOBT (RR 0.68, CI 0.56-0.82) and biennial FOBT (RR 0.78, CI 0.65-0.93) reduced colorectal cancer mortality. As for all-cause mortality, a reduction was not observed for either annual or biennial screening.

Shaukat et al. NEJM 2013; 369:1106-1114

Front 471

What is the most common causative organism in infective endocarditis in patients with HIV?

Back 471

Staph aureus.

Front 472

A patient without HIV presents to your office and has been having fevers, a loud murmur, and night sweats. What is the most common cardiovascular diagnosis causing this condition?

Back 472

Mitral valve prolapse. Especially in patients with mitral valve regurgitation or thickened mitral valve leaflets.

Front 473

What are the relative rates of infection of prosthetic heart valve with infective endocarditis - mechanical vs bioprosthetic?

Back 473

Although mechanical heart valves are probably at higher risk for infection than are bio- prostheses during the first three months after surgery, the rates of infection for the two valve types converge later and are similar at five years.

Front 474

What are the Dukes criteria for infective endocarditis?

Back 474

BE FEVEER
(*BE - Bacterial Endocarditis)
Major:
B = blood culture +ve >2 times 12 hr part
E = Endocardial involvement from Echo
Minor:
F = Fever
E = Echo findings (not fulfilling a major)
V = Vascular findings
EE = Evidences from microbiological/immunology (2 evidences)
R = Risk factors/predisposing factors - drug abuse, valvular diseases

Front 475

Your patient with infective endocarditis is started on antibiotics and is persistently febrile. When should you expect a defervescence from the antibiotics? When is it abnormally prolonged and what is in your differential?

Back 475

Most cases of infective endocarditis should defervesce 2-3 days after the initiation of antibiotics. The most common causes of persistent fever (more than 14 days) are the extension of infec- tion beyond the valve (often with myocardial abscess), focal metastatic infection, drug hypersensitivity (par- ticularly if the fever resolves and then recurs), or a nosocomial infection or other complication of hos- pitalization, such as pulmonary embolism.

Front 476

Your patient with a prosthetic valve is admitted with infective endorcarditis and outside cultures reveal a negative blood culture. What antibiotics do you start and how do you decide?

Back 476

Therapy for culture-negative prosthetic-valve endocarditis within the initial 12 months after valve replacement often includes at least vancomycin and gentamicin. For pa- tients with prosthetic-valve endocarditis that begins 12 months or more after valve surgery, ceftriaxone or cefotaxime could be added to cover for so-called HACEK organisms

Front 477

Indications for surgery in patients with native valve endocarditis.

Back 477

• Valve stenosis or regurgitation leading to heart failure.
• Aortic or mitral regurgitation with hemodynamic evidence of elevated left ventricular end-diastolic or atrial pressures such as premature closure of the mitral valve with aortic regurgitation, rapid decelerating mitral regurgitation signal by continuous wave Doppler (v-wave cutoff sign), or moderate to severe pulmonary hypertension.
• IE due to fungal or other highly resistant organisms.
• Complications such as heart block, annular or aortic abscess, or destructive penetrating lesions such as fistula from the sinus of Valsalva to the right or left atrium or right ventricle, mitral leaflet perforation with IE of the aortic valve, or infection in annulus fibrosis.
Class IIa recommendation:
• Recurrent emboli and persistent vegetations despite appropriate antibiotic therapy.
Class IIb recommendation:
• Mobile vegetations larger than 10 mm with or without emboli.

Front 478

Clinical manifestations of Hemophagocytic syndrome.

Back 478

Hemophagocytic syndrome can masquerade as cirrhosis with ascites. These patients have fever, jaundice, and hepatosplenomegaly, usually in the setting of lymphoma or leukemia.

Front 479

Is there any cutoff coagulation parameter at which paracentesis is contraindicated?

Back 479

There is no data-supported cutoff of coagulation parameters beyond which paracentesis should be avoided.
Runyon BA. Paracentesis of ascitic fluid: a safe procedure. Arch Intern Med 1986;146:2259-2261.

Front 480

Where is the safest place to perform paracentesis?

Back 480

The abdominal wall in the left lower quadrant, 2 finger breadths (3 cm) cephalad and 2 finger breadths medial to the anterior superior iliac spine, has been shown to be thinner and with a larger pool of fluid than the midline and is usually a good choice for needle insertion for performance of a therapeutic paracentesis.

Front 481

What risk are you running if you perform paracentesis in the RLQ?

Back 481

The right lower quadrant may be a suboptimal choice in the setting of a dilated cecum (due to lactulose) or an appendectomy scar.

Front 482

What vessels do you avoid in performed abdominal paracentesis?

Back 482

The area of the in- ferior epigastric arteries should be avoided; these ves- sels are located midway between the pubis and anterior superior iliac spines and then run cephalad in the rec- tus sheath. Visible collaterals should also be avoided.

Front 483

What is the benefit of alcohol cessation in cirrhosis?

Back 483

Child-Pugh C cirrhosis due to alcohol and who stop drinking have an approximately 75% 3-year survival, but all those who continue to drink die in 3 years.
Veldt BJ, Laine F, Guillogomarc'h A, Lauvin L, Boudjema K, Messner M, Brissot P, et al. Indication of liver transplantation in severe alcoholic liver cirrhosis: quantitative evaluation and optimal timing. J Hepatol 2002;36:93-98.

Front 484

What is the role of anticoagulation in acute portal vein thrombosis (PVT)?

Back 484

As opposed to chronic PVT, in the acute setting, anticoagulation is postulated to increase rates of recanalization of the portal vein, helping to lower portal pressures and prevent intestinal ischemia. However, the efficacy and safety of this strategy has been debated, especially in the context of cirrhosis. In one retrospective study, data on 55 patients with cirrhosis and acute or subacute PVT who were placed on anticoagulation were analyzed. Partial or complete recanalization occurred in 60% of patients, with increased rates in patients anticoagulated earlier. Only five patients developed bleeding complications. In patients who stopped anticoagulation, 39% had re-thrombosis. This study implies that anticoagulation is safe and efficacious, but must be continued in the setting of acute PVT and cirrhosis to prevent re-thrombosis.

Delgado et al. Clin Gastroenterol Hepatol. 2012 Jul;10(7):776-83

Front 485

What is the relationship of tachycardia causing worsening hypoxia?

Back 485

At rest, blood transverses the lung relatively slowly so there is time for oxygenation to occur, even in the setting of a disease causing diffusion limitation (e.g. ILD, COPD). With exercise, there is an increase in cardiac output and blood transverses the lungs more quickly. In healthy individuals the body compensates by having pulmonary capillaries dilate, increasing surface area leading to increased gas exchange. In patients with diffusion limitation with a subsequent increase in cardiac output, there is less time for oxygenation resulting in worsening hypoxia.

Harrisons Principles of Internal Medicine. 2011, 18th Ed. Disorders of the Respiratory System.

Front 486

How is acquired C1 esterase deficiency diagnosed?

Back 486

Acquired C1 esterase deficiency should be suspected in patients with angioedema without urticaria. It presents with classic swelling or can manifest as abdominal pain and bloating. Classically, patients have a low C4 level, low C1q level, and a low or normal C1 inhibitor antigenic level. It is generally associated with lymphoproliferative disorders, as they create antibodies that increase C1 consumption. It can be associated with autoimmune diseases such as lupus and chronic infections, but this is very rare and the pathophysiology is poorly understood.

Cicardi et al. Allergy, Asthma & Clinical Immunology 2010;6:14

Front 487

What are the new Kidney Disease Improving Global Outcomes (KDIGO) guidelines for lipid management in patients with chronic kidney disease (CKD)?

Back 487

In 2013, the new KDIGO guidelines recommended adults greater than 50 years of age who are non-dialysis dependent and have not received a kidney transplant, be initiated on either statin monotherapy or a combination of statin/ezetimibe, if their estimated GFR was less than 60 ml/min/1.73 m2 (Grade 1A recommendation). In adults greater than 50 years old with an estimated GFR greater than 60 ml/min/1.73 m2, they recommended statin monotherapy (Grade 1B recommendation). In adults between 18-49 years old who have not been treated with chronic dialysis or kidney transplantation, recommendations are to treat with a statin if they had one or more of the following: known coronary disease, diabetes mellitus, prior ischemic stroke, or an estimated 10-year incidence of coronary death or non-fatal myocardial infarction greater than 10% (Grade 2A recommendation).

Tonelli M et al. Ann Intern Med 2014;160(3): 182-189

Front 488

What are the signs of baclofen withdrawal?

Back 488

The main risks of oral baclofen administration are related to withdrawal: seizures, psychic symptoms and hyperthermia can occur.

Front 489

What is the mechanism of fenfluramine-induced valvulopathy

Back 489

Although initially thought to be due to elevated circulating levels of serotonin, the underlying mechanism of fenfluramine valvulopathy is likely direct action of fenfluramine and its metabolites on the 5-HT2B receptor found on heart valves.

Rothman et al. Expert opin drug saf 2009;8(3):317-329

Front 490

What is the progression of disease of patients with Loeys-Dietz Syndrome (LDS)?

Back 490

Loeys-Dietz syndrome (LDS) is characterized by vascular findings (cerebral, thoracic, and abdominal arterial aneurysms and/or dissections) and skeletal manifestations (pectus excavatum or pectus carinatum, scoliosis, joint laxity, arachnodactyly, talipes equinovarus). Approximately 75% of affected individuals have LDS type I with craniofacial manifestations and approximately 25% have LDS type II with systemic manifestations of LDS I but minimal or absent craniofacial features.

The natural history of LDS types I and II is characterized by aggressive arterial aneurysms (mean age at death 26.1 years, median age 37 years) and high incidence of pregnancy-related complications including death and uterine rupture. The leading cause of death is dissection of thoracic aorta (67%), abdominal aortic dissection (22%), and intracranial bleeding (7%).

Loeys BL et al. GeneReviews™ [Internet]. Seattle (WA): University of Washington, Seattle; 1993-2014

Front 491

What is the mechanism of lithium-induced hyperparathyroidism?

Back 491

Hyperparathyroidism is a lesser known side effect of chronic lithium therapy. Essentially, lithium makes the parathyroid glands less sensitive to circulating calcium, thus shifting the parathyroid hormone curve to compensate for the misperceived low calcium levels. Rates of hyperparathyroidism in patients on lithium in some studies are up to 7.5 times higher than the normal population. Chronic lithium use is more associated with diffuse hyperplasia of the gland, while short term use is thought to unmask existing parathyroid adenomas.

Khairallah et al. Nature Clinical Practice: Nephrology 2007;3(7):397-404

Front 492

What are the management options for persistent atrial fibrillation?

Back 492

A recent multicenter randomized trial performed by the SARA investigators evaluated the use of catheter ablation versus antiarrhythmic drug therapy in patients with persistent atrial fibrillation. The primary endpoint in this study looked at the recurrence of atrial fibrillation after a three month blanking period that lasted for >24 hours within 12 months of follow up. In total, 146 patients were included and they found, based on an intention to treat analysis, that 69/98 (70.4%) patients in the ablation group and 21/48 (43.7%) patients in the antiarrhythmic group to have absence of recurrence. This is one of the first trials assessing the utility of catheter ablation in patients with persistent atrial fibrillation instead of paroxysmal atrial fibrillation.

Mont L et al. Eur Heart J 2014;35(8):501-7

Front 493

What is the correlation between Kayser Fleischer ring size and disease activity in Wilson's disease?

Back 493

Larger K-F ring size may correlate with the severity of the disease, but not necessarily with the magnitude of urinary copper excretion.

Suvarna JC J Postgrad Med July 2008 Vol 54 Issue 3

Front 494

Does the reduction in Kayser Fleischer ring size predict clinical improvement?

Back 494

It is one of the clinical parameters used in monitoring patients on therapy although its reduction is not necessarily a good predictor of clinical improvement.

Suvarna JC J Postgrad Med July 2008 Vol 54 Issue 3

Front 495

Your patient with wilson's disease has reappearance of Kayser Fleischer rings, what is the significance?

Back 495

Its reappearance while on therapy may indicate non-compliance.

Suvarna JC J Postgrad Med July 2008 Vol 54 Issue 3

Front 496

What is the amount of clinical benefit in lowering blood pressure in patients with HTN?

Back 496

Trials involving patients with stage 1 or 2 hypertension showed that lowering systolic pressure by 10 to 12 mm Hg and diastolic pressure by 5 to 6 mm Hg reduces the risk of stroke by 40 percent, the risk of coronary disease by 16 percent, and the risk of death from any cardiovascular cause by 20%

Front 497

Should patients with IPF be treated with corticosteroids or immunosuppressants?

Back 497

We recommend that patients with IPF should not be treated with corticosteroid monotherapy

Front 498

Should patients with IPF and resting hypoxemia receive long-term oxygen therapy?

Back 498

One study has retrospectively compared survival in a cohort of patients with IPF, many of whom (27%) received oxygen therapy. In multivariate analysis, no survival benefit was demonstrated with oxygen use. This study was limited by its retrospective design.

Front 499

Your patient with IPF suddenly develops acute dyspnea, hypoxia, what is the etiology?

Back 499

IPF exacerbations may occur secondary to pneumonia, pulmonary embolism, pneumothorax, or cardiac failure

Front 500

A 34 yo male with a history of smoking presents with subacute dyspnea. CXR reveals bilateral ground glass opacities. Could this be IPF?

Back 500

Patients with IPF aged less than 50 years are rare; such patients may subsequently manifest overt features of an underlying connective tissue disease that was subclinical at the time IPF was diagnosed

Front 501

What are the occupational exposures associated with IPF?

Back 501

-metal dusts (brass, lead, and steel)
-wood dust (pine)
-Farming
-raising birds
-hair dressing
-stone cutting/polishing
-exposure to livestock
-vegetable dust/animal dust

Front 502

What are the features of UIP on CT scan?

Back 502

honeycombing; basal predominant, peripheral predominant reticular abnormality with multiple layers of honeycombing

Front 503

what are the side effects of naloxone that should be monitored?

Back 503

When naloxone is given to a patient who is hypovolemic, hypotensive, and/or previously (before opioid treatment) in severe pain or stress, high-dose naloxone and/or rapidly infused naloxone (i.e., not titrated) can cause catecholamine-mediated cardiac ar- rhythmias and vasoconstriction.

Front 504

When is the greatest risk of developing anthracycline induced cardiomyopathy?

Back 504

The risk of developing cardiomyopathy is present for any of the anthracyclines, the difference is based on their potency. The greatest risk is present if the total dose is greater than 550mg/m^2 for daunorubicin and 900mg/m^2 for epirubicin.

Front 505

Which chemotherapeutic drug is likely associated with myocardial ischemia/ infarction?

Back 505

5-fluorouracil, especially with co-administration with Cisplatin
Capecitabine (Xeloda) is a prodrug of 5-FU

Front 506

Which chemotherapeutic drug is known to produce bradyarrhythmia?

Back 506

Thalidomide

Front 507

A patient with cancer and hematologic malignancy is being pre-opped and you notice he is on hydroxyurea for thrombocytosis - do you have to stop it?

Back 507

Some patients may be taking hydroxyurea and/or anagrelide
(Agrylin) to assist in the management of the thrombocytosis. In general, hydroxyurea inhibits platelet formation and may be safely continued throughout the perioperative period. Anagrelide inhibits platelet formation and aggregation and may need to be stopped in the perioperative period to avoid bleeding complications.

Front 508

A female patient is 39 yo, is having her second child, and is in her 3rd trimester of pregnancy. You are called for a platelet count of 60. Is this compatible with gestational thrombocytopenia?

Back 508

GT is seen in the mid-second to third trimester of pregnancy and is supposed to represent the extreme variation of the physiologic decrease of the platelet count that is observed during pregnancy. There is no clearly defined minimum value of the platelet count in GT, but counts 70 109/L should raise suspicion of an alternative diagnosis.

Front 509

What is the most common cause of thrombocytopenia in early pregnancy?

Back 509

ITP occurs in 1-2 in 1000 pregnancies, but is the most common
cause of isolated thrombocytopenia in the first and early second
trimesters.

Front 510

Your female patient is 9 weeks pregnant and has a platelet count of 100. It continues to decline over the following weeks. What is the most likely explanation?

Back 510

In women with no history of ITP, platelet counts below
100 109/L early in pregnancy and declining as gestation progresses are more consistent with ITP than with GT. Whenever the platelet count is 50 109/L in the absence of obstetric complications, the diagnosis should be ITP by default.

Front 511

What is the first step in the management of concerning thrombocytopenia?

Back 511

Stop any concerning offending agent and also stop any anticoagulants. Next, examine the peripheral smear

Front 512

Which organisms that cause bacteremia are associated with colonic neoplasms?

Back 512

The association between group D streptococci (GDS), specifically S. bovis/gallolyticus infection and colonic neoplasia is well described. The other organism that has an association is Clostridium septicum. In one study the proportion of patients with colonic neoplasia was significantly higher in the setting of GDS infective endocarditis compared to viridans streptococcal endocarditis (63 versus 18 percent) and was 28% for Clostridium septicum bacteremia. The pathogenesis of the association is unclear. The question is still unresolved if S. bovis/gallolyticus plays an etiological role in the development of colorectal tumors or it is merely a marker of the disease.

Abdulamir et al. Journal of Experimental and Clinical Cancer Research 2011;30:11

Front 513

What are the complications of levamisole-contaminated cocaine?

Back 513

Levamisole, originally developed as an anti-helminthic agent, is commonly used as an adulterant in cocaine - both due to its difficulty in being detected and its ability to potentiate the effects of cocaine. A major side effect of this combination is the induction of an anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitis - remarkable for manifesting both anti-myeloperoxidase and anti-proteinase 3 antibodies. The syndrome has multi-system manifestations, but is known in particular to produce cutaneous vasculitis, arthralgias, and glomerulonephritis.

McGrath et al. Clin J Am Soc Nephrol 2011;6(12):2799-805

Front 514

How does cigarette smoking affect white blood cell count?

Back 514

One of the most commonly under-recognized causes of neutrophilia in the outpatient setting is cigarette smoking. White counts in active smokers are raised by approximately 27% compared to nonsmokers and are 14% higher in those abstinent for less than five years. In a retrospective study looking at 6,138 patients between 30 and 74 years of age, number of pack years smoked, years since quitting, and current number of cigarettes smoked were all independent predictors of absolute neutrophil and lymphocyte counts.

Schwartz et al. Ann Epidemiol 1994;4(3):236-42

Front 515

A young woman presents for the fourth time with wheezing and shortness of breath. Not responding to conventional inhalers. She has wheezing throughout. PFTs, including methacholince challenge are normal. What features are suggestive of vocal cord dysfunction and how do you make the diagnosis?

Back 515

The chest radiograph in this patient showed decreased lung volumes, which is in contrast to hyperinflation that would be expected in acute asthma. Oxygen saturation is typically normal in patients with VCD. Make the diagnosis with direct laryngoscopy.

Front 516

What are the indications for Lung Volume reduction surgery in COPD?

Back 516

The effect of lung volume reduction surgery is larger in patients with predominantly nonhomogeneous upper-lobe disease and limited exercise performance after rehabilitation. The ideal candidate should have an FEV1 between 20% and 35% of predicted, the DLCO no lower than 20% of predicted, hyperinflation, and limited comorbidities.

Front 517

What are the indications for nighttime NIPPV in COPD?

Back 517

Daytime hypercapnia and worsening oxygen desaturation during sleep.

Front 518

What are the indications for lung transplantation in COPD?

Back 518

Lung transplantation should be considered in patients hospitalized with COPD exacerbation complicated by hypercapnia (PCO2 greater than 50 mm Hg) and patients with FEV1 not exceeding 20% of predicted and either homogeneous disease on high-resolution CT scan or DLCO less than 20% of predicted who are at high risk of death after lung volume reduction surgery.

Front 519

What are the common causes of endobronchial obstruction in a young person who never smoked?

Back 519

It occurs most commonly in association with foreign body aspiration, endobronchial obstruction by an indolent tumor such as carcinoid tumor, or secondary to extraluminal compression. Carcinomas, including those causing endobronchial obstruction, tend to grow very quickly, resulting in patient treatment (or death) before they can cause focal bronchiectasis.

Front 520

A patient is admitted to ICU, intubated with propofol and etomidate and succinylcholine. Sedated with lorazepam and fentanyl. Later becomes hypertensive, tachycardic, febrile 104, and rigid with CPK in 1000s. What is the diagnosis?

Back 520

Malignant hyperthermia, which is an inherited skeletal muscle disorder characterized by a hypermetabolic state precipitated by exposure to volatile inhalational anesthetics (halothane, isoflurane, enflurane, desflurane, sevoflurane) and the depolarizing muscle relaxants succinylcholine and decamethonium.

Front 521

What is the clinical tempo of Cryptogenic Organizing Pneumonia?

Back 521

The tempo of the disease process is the key to differentiating cryptogenic organizing pneumonia (COP) from other interstitial lung diseases. Acute or subacute, with symptom onset occurring within 2 months of presentation in three fourths of patients.

Front 522

What are the indications for continuous oxygen (15 hours continuously) in COPD?

Back 522

PO2 less than or equal to 55 mm Hg or oxygen saturation less than or equal to 88%
Po2 less than or equal to 59 mm Hg or oxygen saturation less than or equal to 89% if there is evidence of cor pulmonale, right heart failure, or erythrocytosis (hematocrit greater than 55%).

Front 523

What is the triglyceride level in chylothorax?

Back 523

Always >110

Front 524

What is the LDH in a lymphomatous pleural effusion?

Back 524

Always greater than 1000

Front 525

A patient is six hours post-op and develops hypertension, fever, and muscle rigidity. Whats the treatment and dose?

Back 525

This patient likely has malignant hyperthermia, an inherited skeletal muscle disorder characterized by a hypermetabolic state precipitated by exposure to volatile inhalational anesthetics (halothane, isoflurane, enflurane, desflurane, sevoflurane) and the depolarizing muscle relaxants succinylcholine and decamethonium.
The treatment is dantrolene - a muscle relaxant. Dose is bolus of 1 mg/kg intravenously and then 2 mg/kg every 5 to 10 minutes until the symptoms resolve. Response to dantrolene is not diagnostic of the disorder but is supportive if signs and symptoms resolve quickly.

Front 526

Whats the most reliable sign of malignant hyperthermia in a patient who is immediately post-op?

Back 526

The most reliable initial clinical sign heralding the development of acute MH is hypercarbia resistant to increasing the patient's minute ventilation. Patients developing MH while under anesthesia with spontaneous ventilation develop tachypnea as a response to end-tidal carbon dioxide (ETCO2) >60mm Hg and PaCO2 >65mm Hg; those with controlled ventilation have a rising level of CO2 at fixed or increasing ventilator settings.

Due to the increased level of exhaled CO2, not only does the CO2 absorbent rapidly change color, but the exothermic reaction causes the ventilator absorbent canister to become warm to the touch.

Front 527

What are the indications for A1AT infusion in patients with A1AT deficiency?

Back 527

High-risk phenotype (Pi*Z [protease inhibitor Z])
Plasma AAT levels below 50 to 80 mg/dL (0.5-0.8 g/L)
Nonsmoker or ex-smoker
Likely adherence to the protocol
Airflow obstruction with spirometry
Age at least 18 years

Front 528

How do you distinguish the HRCT findings of lymphangioleiomyomatosis vs emphysema?

Back 528

Although the HRCT appearance of emphysema may mimic LAM, the cystic air spaces that occur in LAM are more uniform in appearance and distribution. 36% of cases of LAM present with spontaneous pneumothorax.

Front 529

What are the caloric requirements for patients in the hospital who are severely malnourished?

Back 529

30 nonprotein kcal/kg/d and 1.0 protein kcal/kg/d to meet the energy expenditures associated with critical illness.

Front 530

What is the pathology of ILD with known connective tissue disease?

Back 530

Sjögren syndrome-associated ILD is not limited to LIP but may also present as usual interstitial pneumonia, nonspecific interstitial pneumonia, organizing pneumonia, and interstitial amyloidosis at open lung biopsy.

Front 531

What is the regulated cabin air pressure minimum during flight? How tightly is this controlled?

Back 531

Cabin pressure must maintained no lower than the air pressure equivalent to an altitude of 8000 ft (2438 m).
Cabin air pressure is not constant during flight. There is a relationship between increasing aircraft altitude and falling cabin air pressure.

Front 532

What is the percent O2 of a plane riding at the minimum cabin air pressure?

Back 532

In air at 8000 ft, the O2 partial pressure is approximately equivalent to that when breathing gas containing 15% O2 at MSL

Front 533

What is an acceptable PaO2 during flight?

Back 533

PaO2 levels to remain above 50-55 mmHg during flight, with supplemental O2 recommended in those suspected to fall below these levels.

Front 534

What is the physiologic hazard of hypoxemia during air flight?

Back 534

The primary associated risks are development of dyspnea and acute hypoxemia-related cardiac events.

Front 535

When are patients deemed fit to travel for air flight without risk for hypoxemia related concerns?

Back 535

Generally, they recommend that patients with a sea level room air PaO2 > 70 mmHg, or pulse oximetry (SpO2) > 95% [12] are fit for travel without further testing based on a stated low risk of altitude-related hypoxemia.

Front 536

Your COPD patients has a baseline P02 of 60mmHg, how do you decide if they can travel on an airplane?

Back 536

Either a low-pressure chamber at 8000ft or breathing hypoxic gas of 15% O2 at sea level pressures. Simulate for ~15min, and a PaO2 > 50-55 mmHg or a SpO2 > 85% is regarded as acceptable, with supplemental O2 suggested for those who fall below these levels.

Front 537

When do you use passive warming for hypothermia?

Back 537

Passive rewarming (use of blankets and insulation) and active external rewarming techniques (warm blankets, heating pads, radiant heat, warm baths, forced warm air) are indicated for mild hypothermia with temperatures from 33.9 °C (93.0 °F) to 36.1 °C (97.0 °F).

Front 538

When you warm the trunk as a treatment for hypothermia?

Back 538

Blankets and insulation can be used for moderate hypothermia except that only the truncal areas should be externally rewarmed. Heat applied to the arms and legs forces cold blood back toward the heart, lungs, and brain, causing the core body temperature to decrease, which can worsen the preexisting hypothermia.

Front 539

When do you choose active internal rewarming for patients with hypothermia?

Back 539

In this patient with severe hypothermia (temperature less than 30.0 °C [86.0 °F]), active internal rewarming measures should be considered, such as warmed intravenous fluids, warm and humid oxygen, peritoneal lavage, and extracorporeal rewarming. Complications of rewarming include rhabdomyolysis, compartment syndromes, disseminated intravascular coagulation, pulmonary edema, and acute tubular necrosis.

Front 540

Whats on the differential for an elevated amylase (even salivary component) on a thoracentesis?

Back 540

pancreatic disease (either acute pancreatitis or pancreaticopleural fistula), malignancy (most commonly adenocarcinoma of the lung), and esophageal perforation

Front 541

What is the most effective therapy for smoking cessation?

Back 541

high-dose patch again but in combination with another therapy, such as nicotine replacement with gum or spray, gives the best long-term cessation rate.

Front 542

What are the contraindications to Bupropion for smoking cessation?

Back 542

Seizures occur in approximately 0.1% of patients who take the drug, and the risk appears to be higher in patients with a *preexisting seizure disorder, anorexia nervosa, or bulimia.*

Front 543

For a pulmonary nodule of 1-2 cm diameter. What kind of sampling method would you choose?

Back 543

There are reported yields of about 90% for nodules of 1 to 2 cm with transthoracic needle aspiration and less that 50% for bronchoscopy.

Front 544

What are organophosphates?

Back 544

Organophosphates are a diverse group of chemicals used in both domestic and industrial settings that include insecticides, nerve gases (soman, sarin, tabun, VX), ophthalmic agents (echothiophate, isoflurophate), and antihelmintics (trichlorfon).

Front 545

What is the molecular target of organophosphate?

Back 545

Organophosphate insecticides inhibit both cholinesterase and pseudocholinesterase activities. The inhibition of cholinesterase activity leads to accumulation of acetylcholine at synapses, causing overstimulation and disruption of neurotransmission in both the central and peripheral nervous systems.

Front 546

What are the signs and symptoms of organophosphate poisoning?

Back 546

Signs and symptoms of organophosphate poisoning include muscarinic effects, nicotinic effects, and central nervous system effects. Muscarinic manifestations include excessive salivation, diarrhea, vomiting, hypersalivation, respiratory distress with bronchorrhea and bronchospasm, abdominal pain, depressed level of consciousness, and muscle fasciculations. The muscarinic signs of organophosphate poisoning can be recalled with the help of the mnemonic DUMBELS—Defecation, Urination, Miosis, Bronchorrhea/Bronchospasm/Bradycardia, Emesis, Lacrimation, Salivation. Nicotinic manifestations include increased muscle weakness, skeletal muscle fasciculations, and respiratory failure secondary to diaphragmatic paralysis. Central nervous system effects include altered mental status and seizures.

Front 547

What is the treatment for organophosphate poisoning?

Back 547

Pralidoxime (2-PAM) reactivates acetylcholinesterase and can reverse the muscle weakness, paralysis, and respiratory depression of organophosphate toxicity.

Front 548

How do you diagnose Vocal cord dysfunction and what are you looking for?

Back 548

Flow volume loops document the inspiratory and expiratory flow by recording the flow while the patient inhales as deeply as possible and then exhales as much as possible. An inspiratory cut-off in flow (flattening of the inspiratory portion of the flow loop) with relatively preserved expiratory flow indicates an extrathoracic variable obstruction that is typical in patients with VCD.

Front 549

When and how can you use neuro specific enolase after cardic arrest?

Back 549

Use it as a marker of neurologic recovery at 48 hours after cardiac arrest. NSE was elevated above 33mcg/mL in 17 of 34 patients, all of whom died without regaining consciousness. Of the remaining 17 patients with an NSE below 33 g/L, 6 regained consciousness.

Front 550

How do you diagnose reactive airway disease presumed to be due to an occupational exposure, such as ammonia?

Back 550

Methacholine challenge testing can be done safely in patients with asthma provided that appropriate guidelines are followed and that the FEV1 is greater than 70% of predicted.

Front 551

What three lab findings help rule out ANCA-associated vasculitis?

Back 551

The ANCA-associated vasculitides are not associated with hypocomplementemia, hypergammaglobulinemia, or high titers of rheumatoid factor.

Front 552

A patient with dermatomyositis is treated with high dose prednisone but fails to respond to therapy over the following months. What is the next step?

Back 552

Evaluation for an occult malignancy is warranted in patients with dermatomyositis who are refractory to treatment, particularly those who are older than 60 years of age.

Front 553

Your patient is started on a statin and develops muscle aches and pains. You stop the statin but the pain persists weeks later. What is the diagnosis?

Back 553

Most statin induced myotoxicity is self-limiting and recovers over weeks to months upon stopping of the statin. There is a series of patients in whom the statin induced myotoxicity has persisted or progressed despite the cessation of statin treatment. These relatively rare cases in the context of statin induced myotoxicity have been described on muscle biopsy as necrotizing autoimmune myopathy (NAM)

Front 554

Which muscle groups do statin induced myopathy typically affect?

Back 554

The muscle symptoms tend to be proximal, symmetrical, generalised, and worse with exercise or the initiation of a new medication.

Front 555

When does statin induced myopathy typically occur with relation to the initiation of the drug?

Back 555

The PRIMO study showed that the median time of onset of muscle symptoms was one month after the initiation of statin treatment or titration to a higher dose, although 15% of those reporting muscle symptoms had symptoms that appeared six months after treatment initiation

Front 556

Which drug is the most common culprit of rhabdo when combined with statin therapy?

Back 556

The incidence of rhabdomyolysis is increased 12-fold when statins are combined with gemfibrozil. The average length of time on statins before the onset of rhabdomyolysis is about one year, but this shortens to one month when statin use is combined with gemfibrozil

Front 557

Severe rheumatoid arthritis, on multiple medications, including prednisone and etanercept. Still has severe symptoms. What do you do?

Back 557

There is evidence that you should switch etanercept to an alternative ant-TNF inhibitor.

Front 558

You have a case of mild rheumatoid arthritis in a patient that drinks significantly. There is no active hepatitis. Do you choose leflunomide, MTX, or Sulfasalazine?

Back 558

Sulfasalazine (or hydroxychloroquine). Methotrexate is a DMARD that is often used in patients with active rheumatoid arthritis but would be contraindicated in a patient with abnormal liver chemistry study results or underlying liver disease, or in those who regularly consume alcoholic beverages. Leflunomide is similarly associated with hepatotoxicity and should be avoided in patients who consume significant amounts of alcohol.

Front 559

Mixed myopathic and neurogenic findings on electromyography?

Back 559

Inclusion body myositis

Front 560

Daily fever that spikes once or twice daily, polyarthritis, and leukocytosis.

Back 560

Adult Onset Stills disease.
First rule out infection and Malignancy.

Front 561

What are the clinical manifestations of scleroderma renal crisis?

Back 561

SRC classically is characterized by the acute onset of severe hypertension, renal failure, and microangiopathic hemolytic anemia. Patients who develop this condition as a result of corticosteroid use often are normotensive but may have blood pressures higher than their normal baseline levels.

Front 562

What is the treatment for scleroderma renal crisis?

Back 562

Prompt initiation of therapy with an angiotensin-converting enzyme inhibitor such as captopril is the treatment of choice for SRC. This therapy should be continued even in patients with significant renal insufficiency, as renal function has been shown to improve even after months of dialysis.

Front 563

Two first line therapies for psoriatic arthritis?

Back 563

Methotrexate and TNF inhibitors.

Front 564

Anti-Smith antibodies are highly specific for SLE but are associated with two conditions.

Back 564

SLE patients with glomerulonephritis and central nervous system disease

Front 565

Treatment for polyarteritis nodosa associated with HBV?

Back 565

High dose prednisone and lamivudine

Front 566

Young adult with MCP pain and 3 days self limited rash?

Back 566

Parvovirus B19

Front 567

Patient with symmetric arthritis, morning stiffness, +RF, and +HCV. What is the treatment?

Back 567

First differentiate. Differentiating between HCV infection-associated arthritis and rheumatoid arthritis is essential, because treatment of these conditions differs greatly. Initiation of effective antiviral treatment is indicated for HCV infection-associated arthritis, whereas careful selection and early initiation of disease-modifying antirheumatic drug therapy is indicated for rheumatoid arthritis.

Front 568

Diagnosis: Polymyositis with extramuscular features?

Back 568

Nearly one third of patients with an inflammatory myopathy have the antisynthetase syndrome. This condition can have an acute or subacute onset and is characterized by fever; fatigue; Raynaud phenomenon; synovitis; interstitial lung disease; and scaly, rough, dry, darkened, cracked horizontal lines that develop on the palmar and lateral aspects of the fingers that are known as "mechanic's hands."

Front 569

Most common antibody in the antisynthetase syndrome?

Back 569

Patients with antisynthetase syndrome have antisynthetase antibodies that are specific for an inflammatory myopathy. The most common antisynthetase antibody is the anti-Jo-1 antibody.

Front 570

Patient stopped atorvastatin after developing myalgias and an elevated CK 6 mos ago. She has a persistently elevated CK now. Whats the next step?

Back 570

MRI and Biopsy.

Front 571

Your patient with dermatomyositis comes for routine labs and CK has nearly tripled. What does this indicate?

Back 571

Because an increase in creatine kinase levels often precedes a decrease in muscle strength, this patient's normal results on muscle strength testing do not preclude active myositis.

Front 572

Patient with lupus comes in feeling well but on labs and exam she has hypertension, ankle edema, hematuria, proteinuria, hypoalbuminemia, Creatinine is 1.0, and erythrocyte casts on urinalysis. What do you do?

Back 572

This is highly suggestive of lupus nephritis despite the absence of renal insufficiency. To prevent irreversible renal damage, early treatment with a high-dose corticosteroid such as prednisone is indicated for patients whose condition raises strong suspicion for lupus nephritis.

Front 573

Woman with SLE has APLS and loses a baby. Her lupus nephritis is currently flaring but she wants to have another child. How do you proceed?

Back 573

Cyclophosphamide therapy, when combined with high-dose corticosteroids, is the treatment of choice in patients with lupus nephritis. Therefore, effective management of this patient's reproductive health consists of trying to avoid pregnancy during cyclophosphamide therapy and while SLE is active as well as trying to maintain fertility. The best option is leuprolide injections (OCPs will cause clotting).

Front 574

Tracheal tenderness and stridor and eye redness associated with impending respiratory failure. Dx?

Back 574

Relapsing polychondritis - tracheal inflammation and subglottic stenosis, which often cause tracheal and/or airway collapse in patients

Front 575

SLE patient gets pregnant. She is on hydroxychloroquine - no recent flares, labs look good. What do you do?

Back 575

Patients with SLE whose disease has been quiescent for at least 6 months, during which time they either did not use medications for SLE or used medications that can safely be continued during pregnancy, generally have positive pregnancy outcomes.

Front 576

Asymmetric pulses and blood pressure in a patient with hypertension. Dx? Cause of hypertension?

Back 576

Takayasu's arteritis associated with renal artery stenosis.

Front 577

What size induration do you treat LTBI in a patient about to go onto TNF inhibitor?

Back 577

The Centers for Disease Control and Prevention recommends treatment of latent tuberculosis infection for all patients planning to take a TNF-α inhibitor who have a PPD result of 5 mm or more of induration or a positive interferon-γ release assay.

Front 578

Post-arthroplasty patient of hip has significant lateral sided pain for past week. There is no fever or WBC. What is the most likely diagnosis?

Back 578

Pain is the predominant or only symptom in patients with prosthetic joint infection, and fever and leukocytosis are frequently absent.

Front 579

How frequently do patients in the chronic inactive carrier state convert HBsAg negative?

Back 579

HBsAg loss and seroconversion to anti-HBs antibody may occur spontaneously in 1-3% of cases per year, usually after several years with persistently undetectable HBV DNA

Front 580

An 18 yo male has a single tonic clonic seizure. Labs, EEG, and Imaging are normal. What do you prescribe?

Back 580

After a single unprovoked seizure, the risk of recurrence in the subsequent 2 years has been reported to be 30% to 40%. If a second seizure occurs in the future, the recurrence risk is greater than 60%, and antiepileptic medical therapy should be recommended at that time.

Front 581

What is the agent for menstrually related migraines?

Back 581

mefenamic acid for perimenstrual prophylaxis, with treatment starting 2 days prior to the onset of flow or 1 day prior to the expected onset of the headache and continuing for the duration of menstruation

Front 582

Clinical triad of Lambert Eaton Syndrome?

Back 582

proximal upper and lower limb weakness, the presence of autonomic symptoms (dry eyes/mouth, erectile dysfunction), and the finding of absent deep tendon reflexes on examination

Front 583

Antibodes associated with Lambert Eaton Syndrome?

Back 583

voltage-gated P/Q-type calcium channel receptors

Front 584

A patient presents with Parkinsoninan type features. What distinguishes Multiple System Atrophy? What is the clinical triad?

Back 584

The dysautonomia is a distinguishing feature. Clinical triad: autonomic nervous system (orthostatic hypotension, erectile dysfunction, constipation)

the extrapyramidal system (rigidity, impaired gait)

cerebellum (limb ataxia)

Front 585

A patient is treated for migraine in the ER with prochlorperazine. He develops torticollis, flushing , and inability to move the neck to the right. What is the treatment?

Back 585

Intravenous anticholinergic agents, such as benztropine or diphenhydramine, are the treatment of choice in the acute treatment of dystonic reactions. Benzodiazepine medications can also be helpful in the acute setting. Oral anticholinergic medications are continued for 48 to 72 hours to prevent relapse.